case study of ischemic heart disease

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Article Contents

Introduction, case presentation.

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Clinical case: heart failure and ischaemic heart disease

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Giuseppe M C Rosano, Clinical case: heart failure and ischaemic heart disease, European Heart Journal Supplements , Volume 21, Issue Supplement_C, April 2019, Pages C42–C44, https://doi.org/10.1093/eurheartj/suz046

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Patients with ischaemic heart disease that develop heart failure should be treated as per appropriate European Society of Cardiology/Heart Failure Association (ESC/HFA) guidelines.

Glucose control in diabetic patients with heart failure should be more lenient that in patients without cardiovascular disease.

Optimization of cardiac metabolism and control of heart rate should be a priority for the treatment of angina in patients with heart failure of ischaemic origin.

This clinical case refers to an 83-year-old man with moderate chronic obstructive pulmonary disease and shows that implementation of appropriate medical therapy according to the European Society of Cardiology/Heart Failure Association (ESC/HFA) guidelines improves symptoms and quality of life. 1 The case also illustrates that optimization of glucose metabolism with a more lenient glucose control was most probably important in improving the overall clinical status and functional capacity.

The patient has family history of coronary artery disease as his brother had suffered an acute myocardial infarction (AMI) at the age of 64 and his sister had received coronary artery by-pass. He also has a 14-year diagnosis of arterial hypertension, and he is diabetic on oral glucose-lowering agents since 12 years. He smokes 30 cigarettes per day since childhood.

In February 2009, after 2 weeks of angina for moderate efforts, he suffered an acute anterior myocardial infarction. He presented late (after 14 h since symptom onset) at the hospital where he had been treated conservatively and had been discharged on medical therapy: Atenolol 50 mg o.d., Amlodipine 2.5 mg o.d., Aspirin 100 mg o.d., Atorvastatin 20 mg o.d., Metformin 500 mg tds, Gliclazide 30 mg o.d., Salmeterol 50, and Fluticasone 500 mg oral inhalers.

Four weeks after discharge, he underwent a planned electrocardiogram (ECG) stress test that documented silent effort-induced ST-segment depression (1.5 mm in V4–V6) at 50 W.

He underwent a coronary angiography (June 2009) and left ventriculography that showed a not dilated left ventricle with apical dyskinesia, normal left ventricular ejection fraction (LVEF, 52%); occlusion of proximal LAD, 60% stenosis of circumflex (CX), and 60% stenosis of distal right coronary artery (RCA). An attempt to cross the occluded left anterior descending (LAD) was unsuccessful.

He was therefore discharged on medical therapy with: Atenolol 50 mg o.d., Atorvastatin 20 mg o.d., Amlodipine 2.5 mg o.d., Perindopril 4 mg o.d., oral isosorbide mono-nitrate (ISMN) 60 mg o.d., Aspirin 100 mg o.d., metformin 850 mg tds, Gliclazide 30 mg o.d., Salmeterol 50 mcg, and Fluticasone 500 mcg b.i.d. oral inhalers.

He had been well for a few months but in March 2010 he started to complain of retrosternal constriction associated to dyspnoea for moderate efforts (New York Heart Association (NYHA) II–III, Canadian Class II).

For this reason, he was prescribed a second coronary angiography that showed progression of atherosclerosis with 80% stenosis on the circumflex (after the I obtuse marginal branch) and distal RCA. The LAD was still occluded.

After consultation with the heart team, CABG was avoided because surgical the risk was deemed too high and the patient underwent palliative percutaneous coronary intervention (PCI) of CX and RCA. It was again attempted to cross the occlusion on the LAD. But this attempt was, again, unsuccessful. Collateral circulation from posterior interventricular artery (PDL) to the LAD was found. The pre-PCI echocardiogram documented moderate left ventricular dysfunction (EF 38%), the pre-discharge echocardiogram documented a LVEF of 34%. Because of the reduced LVEF, atenolol was changed for Bisoprolol (5 mg o.d.).

At follow-up visit in December 2012, the clinical status and the haemodynamic conditions had deteriorated. He complained of worsening effort-induced dyspnoea/angina that now occurred for less than a flight of stairs (NYHA III). On clinical examination clear signs of worsening heart failure were detected ( Table  1 ). His medical therapy was modified to: Bisoprolol 5 mg o.d., Atorvastatin 20 mg o.d., Amlodipine 2.5 mg o.d., Perindopil 5 mg o.d., ISMN 60 mg o.d., Aspirin 100 mg o.d., Metformin 500 mg tds, Furosemide 50 mg o.d., Gliclazide 30 mg o.d., Salmeterol 50 mcg oral inhaler, and Fluticasone 500 mcg oral inhaler. A stress perfusion cardiac scintigraphy was requested and revealed dilated ventricles with LVEF 19%, fixed apical perfusion defect and reversible perfusion defect of the antero-septal wall (ischaemic burden <10%, Figure  1 ). He was admitted, and an ICD was implanted.

Clinical parameters during follow-up visits

Myocardial perfusion scintigraphy and left ventriculography showing dilated left ventricle with left ventricular ejection fraction 19%. Reversible perfusion defects on the antero-septal wall and fixed apical perfusion defect.

In March 2013, he felt slightly better but still complained of effort-induced dyspnoea/angina (NYHA III, Table  1 ). Medical therapy was updated with bisoprolol changed with Nebivolol 5 mg o.d. and perindopril changed to Enalapril 10 mg b.i.d. The switch from bisoprolol to nebivolol was undertaken because of the better tolerability and outcome data with nebivolol in elderly patients with heart failure. Perindopril was switched to enalapril because the first one has no indication for the treatment of heart failure.

In September 2013, the clinical conditions were unchanged, he still complained of effort-induced dyspnoea/angina (NYHA III) and did not notice any change in his exercise capacity. His BNP was 1670. He was referred for a 3-month cycle of cardiac rehabilitation during which his medical therapy was changed to: Nebivolol 5 mg o.d., Ivabradine 5 mg b.i.d., uptitrated in October to 7.5 b.i.d., Trimetazidine 20 mg tds, Furosemide 50 mg, Metolazone 5 mg o.d., K-canrenoate 50 mg, Enalapril 10 mg b.i.d., Clopidogrel 75 mg o.d., Atorvastatin 40 mg o.d., Metformin 500 mg b.i.d., Salmeterol 50 mcg oral inhaler, and Fluticasone 500 mcg oral inhaler.

At the follow-up visit in January 2014, he felt much better and had symptomatically, he no longer complained of angina, nor dyspnoea (NYHA Class II, Table  1 ). Trimetazidine was added because of its benefits in heart failure patients of ischaemic origin and because of its effect on functional capacity. Ivabradine was added to reduce heart rate since it was felt that increasing nebivolol, that was already titrated to an effective dose, would have had led to hypotension.

He missed his follow-up visits in June and October 2014 because he was feeling well and he had decided to spend some time at his house in the south of Italy. In January and June 2015, he was well, asymptomatic (NYHA I–II) and able to attend his daily activities. He did not complain of angina nor dyspnoea and reported no limitations in his daily activities. Unfortunately, in November 2015 he was hit by a moped while on the zebra crossing in Rome and he later died in hospital as a consequence of the trauma.

This case highlights the need of optimizing both the heart failure and the anti-anginal medications in patients with heart failure of ischaemic origin. This patient has improved dramatically after the up-titration of diuretics, the control of heart rate with nebivolol and ivabradine and the additional use of trimetazidine. 1–3 All these drugs have contributed to improve the clinical status together with a more lenient control of glucose metabolism. 4 This is another crucial point to take into account in diabetic patients, especially if elderly, with heart failure in whom aggressive glucose control is detrimental for their functional capacity and long-term prognosis. 5

IRCCS San Raffaele - Ricerca corrente Ministero della Salute 2018.

Conflict of interest : none declared. The authors didn’t receive any financial support in terms of honorarium by Servier for the supplement articles.

Ponikowski P , Voors AA , Anker SD , Bueno H , Cleland JG , Coats AJ , Falk V , González-Juanatey JR , Harjola VP , Jankowska EA , Jessup M , Linde C , Nihoyannopoulos P , Parissis JT , Pieske B , Riley JP , Rosano GM , Ruilope LM , Ruschitzka F , Rutten FH , van der Meer P ; Authors/Task Force Members. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) Developed with the Special Contribution of the Heart Failure Association (HFA) of the ESC . Eur J Heart Fail 2016 ; 18 : 891 – 975 .

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Rosano GM , Vitale C. Metabolic modulation of cardiac metabolism in heart failure . Card Fail Rev 2018 ; 4 : 99 – 103 .

Vitale C , Ilaria S , Rosano GM. Pharmacological interventions effective in improving exercise capacity in heart failure . Card Fail Rev 2018 ; 4 : 1 – 27 .

Seferović PM , Petrie MC , Filippatos GS , Anker SD , Rosano G , Bauersachs J , Paulus WJ , Komajda M , Cosentino F , de Boer RA , Farmakis D , Doehner W , Lambrinou E , Lopatin Y , Piepoli MF , Theodorakis MJ , Wiggers H , Lekakis J , Mebazaa A , Mamas MA , Tschöpe C , Hoes AW , Seferović JP , Logue J , McDonagh T , Riley JP , Milinković I , Polovina M , van Veldhuisen DJ , Lainscak M , Maggioni AP , Ruschitzka F , McMurray JJV. Type 2 diabetes mellitus and heart failure: a position statement from the Heart Failure Association of the European Society of Cardiology . Eur J Heart Fail 2018 ; 20 : 853 – 872 .

Vitale C , Spoletini I , Rosano GM. Frailty in heart failure: implications for management . Card Fail Rev 2018 ; 4 : 104 – 106 .

• myocardial ischemia
• cardiac rehabilitation
• heart failure
• older adult

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A monthly publication of the Brazilian Society of Cardiology and considered the main channel for the promotion of Brazilian cardiovascular research.

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Arq. bras. cardiol. 2018; 111(6): 860-863, case 6 – woman with ischemic heart disease admitted due to chest pain and shock.

Rafael Amorim Belo Nunes , Hilda Sara Montero Ramirez , Vera Demarchi Aiello

DOI: 10.5935/abc.20180231

Clinical aspects

This patient is a 67-year-old woman with cardiovascular risk factors and ischemic cardiomyopathy, with severe left ventricular systolic dysfunction. Cardiac catheterization disclosed multivessel coronary disease and apical akinesis with an intracavitary thrombus. During outpatient follow-up, clinical treatment was chosen, possibly influenced by the patient’s clinical status, as well as the characteristics of the coronary anatomy.

The indication of surgical treatment with myocardial revascularization in patients with coronary heart disease with heart failure and severe left ventricular systolic dysfunction is still debatable, but recent data from the STICH study suggest a long-term survival benefit in patients undergoing myocardial revascularization.

Keywords: Cardiac Catheterization;Thromboembolism ; Chest Pain ; Myocardial Infarction ; Myocardial Ischemia ; Shock, Cardiogenic

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• Published: 14 September 2024

A global analysis of the burden of ischemic heart disease attributable to diet low in fiber between 1990 and 2019

• Nana Wei 1 ,
• Lichao Wang 2 ,
• Bi Tang 2 ,
• Yuli Huang 2 &
• Ling Xuan 2  

BMC Cardiovascular Disorders volume  24 , Article number:  491 ( 2024 ) Cite this article

Metrics details

Ischemic heart disease (IHD) represents a major cardiovascular condition heavily influenced by dietary factors. This study endeavors to assess the global, regional, and temporal impact of low-fiber diets on the burden of IHD.

Leveraging data from the Global Burden of Disease (GBD) 2019 study, we analyzed the worldwide burden of IHD resulting from diet low in fiber using indices including death and disability-adjusted life years (DALY). This burden was further segmented based on variables including regions and countries. To track the evolution from 1990 to 2019, we utilized the Joinpoint regression model to estimate the temporal trend of IHD burden stemming from low-fiber diets.

In 2019, a total of 348.85 thousand (95%UI: 147.57, 568.31) deaths and 7942.96 thousand (95%UI: 3373.58,12978.29) DALY (95% UI: 707.88, 1818) of IHD were attributed to diet low in fiber globally. These figures correspond to 3.82% of all IHD deaths and 4.36% of total IHD DALYs. The age-standardized death and DALY rates per 100,000 individuals were 4.48 (95% UI: 1.90,7.27) and 97.4(95%UI: 41.44, 158.88) respectively. However, significant regional disparities emerged in these age-standardized rates, with South Asia and Central Asia experiencing the highest rates. Between 1990 and 2019, we observed that most regions displayed a downward trend of the age-standardized DALY and death rate of IHD resulting from low-fiber diets, except for Central Sub-Saharan Africa and Southern Sub-Saharan Africa.

Our analysis underscores the substantial toll of IHD associated with low-fiber diets, particularly considering the significant regional variations. Therefore, it is imperative to sustain efforts to implement effective measures aimed at enhancing fiber intake worldwide, particularly in countries with lower socio-demographic indices.

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Introduction

Ischemic heart disease (IHD) stands as a prevalent cardiovascular condition that poses a significant threat to global public health. According to recent statistics, in 2019, the number of individuals afflicted with IHD reached 197 million, representing 16.17% of all deaths and accounting for 7.19% of disability-adjusted life-years (DALY) globally [ 1 ]. Given these figures, primary prevention becomes paramount in mitigating or eliminating risk factors that influencing IHD.

Emerging studies showed that dietary compounds can significantly impact cardiovascular diseases in diverse manners [ 2 ]. Notably, dietary fiber, considered the seventh crucial nutrient for the body, is a vital and health-promoting component of our diet. It is widely acknowledged that sufficient dietary fiber intake aids in inhibiting the development and progression of cardiovascular diseases [ 3 ]. Further evidence has highlighted the impact of dietary fiber in reducing the occurrence and development of IHD [ 4 , 5 , 6 ]. For instance, a prospective study spanning 12.6 years and involving 490,311 subjects across 10 European countries revealed that an increment of 10 g of dietary fiber intakes per day correlated with 9% decrement in the risk of IHD [ 6 ]. Mechanistically, dietary fiber contributes to reducing IHD risk by lowering serum cholesterol levels, blood pressure, as well as levels of inflammatory and oxidative stress markers, critical factors in the progression of IHD [ 7 , 8 ]. It has also demonstrated that dietary fiber enhances gut microbiota diversity, which is linked to the onset of cardiovascular diseases [ 9 ]. Nevertheless, it is noteworthy that most individuals fail to meet the recommended daily fiber intake worldwide.

However, so far, no studies have quantified the global burden of IHD associated with a low-fiber diet. Moreover, existing research exhibits variations in observation durations, analytical methodologies, and model specifications, posing challenges in comparing their findings. Fortunately, the GBD study provides a platform to assess the diet low in fiber associated IHD burden globally, utilizing standardized techniques [ 10 , 11 ]. In particular, the burden of IHD is more severe among the elderly population [ 12 , 13 ]. In the context of global aging, analyzing modifiable dietary risk factors for IHD is of great significance for policy formulation and disease prevention.

In summary, this study employed the GBD 2019 database to fulfill three primary goals: firstly, to quantify the worldwide impact of IHD stemming from a diet deficient in fiber, and categorize this impact based on variables including GBD regions and countries; secondly, to examine the trends in IHD burden associated with low-fiber diets from 1990 to 2019. The insights gained from this research could aid policymakers in pinpointing critical areas and crafting effective public health policies.

In 2020, the GBD Study conducted a thorough scientific evaluation of the diverse diseases, and risk factors worldwide, spanning 204 countries and territories from 1990 to 2019 [ 10 , 11 ]. The global survey encompassed the whole world into 21 regions and further grouped into seven super regions. Moreover, the study stratified the nations into five developmental tiers, using a socio-demographic index (SDI). Our retrieval of data from the Institute for Health Metrics and Evaluation encompassed the number of DALYs (Disability-Adjusted Life Years) and deaths attributed to IHD caused by a low-fiber diet, globally, across geographical regions, SDI regions, and specific countries between 1990 and 2019, along with their age-standardized rates.

Estimation process

The primary source of dietary fiber data utilized by GBD 2019 is derived from nutrition surveys such as 24-hour diet recall. Furthermore, GBD 2019 study characterized a low-fiber diet as consuming less than 21–22 g of fiber daily on average, encompassing various sources such as fruits and grains [ 10 , 11 ]. IHD was defined as I20 to I25. Elsewhere [ 10 , 11 ], the GBD methods for estimating the disease burden attributed to specific factors were outlined. In brief, based on a large number of literature reviews and meta-analysis studies, GBD 2019 estimated the relative risk (RR) of IHD caused by a low-fiber diet and used the population attributable fraction (PAF) to estimate its degree of harm to the population. The average exposure level of the risk factor was assessed utilizing a Bayesian meta-regression framework and a spatiotemporal Gaussian process regression model. By multiplying the PAF by the number of IHD death and DALY, the number of IHD death and DALY caused by a low-fiber diet were obtained. The standardization of rates was calculated based on the World Standard Population published by the World Health Organization.

Statistical analysis

We presented comprehensive data accompanied by 95% uncertainty intervals (UI) concerning the IHD death and DALY, resulting from diets deficient in fiber globally, as well as categorized based on age, gender, geographical regions, and nations. Furthermore, the research utilized a Spearman correlation analysis to investigate the link between the SDI and the age-standardized IHD mortality and DALY rates, which are attributable to diets lacking in fiber. To analyze the temporal trends of the low-fiber diets associated IHD burden from 1990 to 2019, a Joinpoint regression model was utilized [ 14 ]. The research then determined the average annual percent change (AAPC) and its associated 95% confidence intervals [ 14 ]. These trends were subsequently classified as increasing (AAPC greater than 0), decreasing (AAPC less than 0), or remaining stable (where the 95% confidence interval encompassed 0). The Joinpoint Regression Program and R software used to perform data analyses. Statistical significance was defined as a P -value less than 0.05.

Global burden of IHD attributable to diet low in fiber in 2019

In 2019, 7942.96 thousand (95%UI: 3373.58,12978.29) DALYs and 348.85 thousand (95%UI: 147.57, 568.31) deaths of IHD were related with diet low in fiber globally, accounting for 4.36% (95%UI: 1.81%,7.02%) DALY and 3.82% (95%UI: 1.58%,6.15%) death of total IHD, respectively (Table  1 ). In terms of age-standardized rate, the DALY rate changed from 176.79(95%UI: 76.41, 278.30, per 100,000 population) in 1990 to 97.4(95%UI:41.44,158.88, per 100,000 population) in 2019, with AAPC of -2.02% (95%CI: -2.06%, -1.98%). Also, the death rate significantly decreased (AAPC: -2.26%,95%CI: -2.29%, -2.22%), reaching 4.48(95%UI: 1.90, 7.27) in 2019 (Fig.  1 ).

Temporal trend in IHD burden attributable to diet low in fiber in different regions from 1990 to 2019(red line indicated age-standardized death rate (per 100000 people), while blue line meant the age-standardized DALY rate (per 100000 people))

The age-standardized DALY and death rates of IHD due to diet low in fiber were 128.43(95%UI: 54.67,209.83) and 5.56(95%UI: 2.36,9.18) in males, while were 67.91(95% UI: 28.70,111.52) and 3.35(95%UI:1.47,5.86) in females. Meanwhile, the age-specific DALY and death rates of diet low in fiber-related IHD increased with aging in both genders (Fig. S1 ). The number of DALY of IHD resulting from diet low in fiber was highest in age groups of 50–54 in males, while in age groups of ≥ 80 years in females. While, the number of deaths of IHD associated with diet low in fiber was highest in age groups of ≥ 80 years in both genders.

The burden of IHD attributable to diet low in fiber by regions

The results were shown in Table  1 . Among the 21 regions, the number (thousand) of diet low in fiber-related IHD DALYs ranged from 2.05(95%UI:0.94,3.94) in Oceania to 2645.65 (95%UI:1153.86,4363.78) in South Asia. While, Central Asia (240.37, 95% UI:87.15,419.51) has the largest age-standardized DALY rate of IHD associated with diet low in fiber, followed by Southeast Asia (231.53,95% UI: 111.36, 351.70), South Asia (175.93,95%UI:76.41,289.75) Eastern Europe (168.78, 95%UI: 59.96, 299.72). Western Sub-Saharan Africa (20.20, 95% UI: 9.41,34.86) has the lowest age-standardized DALY rate of IHD associated with diet low in fiber (Fig.  1 ). Similarly, the highest age-standardized death rate of IHD associated with diet low in fiber was also observed in Central Asia (13.15,95% UI: 4.74,22.81), and the lowest was observed in Oceania (1.07,95% UI: 0.52,1.95). The number (thousand) of diet low in fiber-related IHD deaths ranged from 0.07(95%UI:0.03,0.12) in Oceania to 95.23 (95%UI: 42.04, 155.49) in South Asia.

Between 1990 and 2019, most regions displayed a downward trend of the age-standardized DALY and death rate of IHD associated with diet low in fiber, except for Central Sub-Saharan Africa and Southern Sub-Saharan Africa (Fig.  1 ). In Central Sub-Saharan Africa, both of the DALY and death rates of diet low in fiber-related IHD significantly increased, with AAPC of 0.93% (95%CI: 0.88%,0.98%) and 1.09% (95%CI: 1.04%,1.14%). Likewise, in Southern Sub-Saharan Africa, the death rate of IHD resulting from diet low in fiber also significantly increased (AAPC: 0.24%,95%CI: 0.11%, 0.39%), while the DALY rate remained stable (AAPC: -0.03%,95%CI: -0.15%, 0.09%). Among the countries which had a downward trend of the age-standardized DALY and death rate of IHD resulting from diet low in fiber, the largest and smallest decrease was observed in Australasia (AAPC: -4.79%,95%CI: -4.83%, -4.74% and − 4.67%,95%CI: -4.73%, -4.62%) and Eastern Europe (AAPC: -0.32%, 95%CI: -0.48%, -0.14% and − 0.51%,95%CI: -0.72%, -0.26%), respectively.

The burden of IHD attributable to diet low in fiber by countries and territories

The number (thousand) of IHD DALYs (1627.40,95%UI: 598.48, 2895.89) and deaths (59.30,95%UI:22.07,105.77) resulting from diet low in fiber was largest in India, followed by China, United States of America, and Indonesia (Table S1 ). As for the age-standardized DALY rate of IHD resulting from diet low in fiber, Mongolia tops the first with 613.76(95%UI: 303.14, 958.17) DALYs, followed by Afghanistan, Tajikistan, Yemen and Uzbekistan. Mongolia also has the largest age-standardized death rate of IHD attributable to diet low in fiber (Fig.  2 ). Table S1 listed the results of the temporal trend of IHD resulting from diet low in fiber for each country between 1990 and 2019. A notable increase in the age-standardized DALY rate is evident in 30 countries and territories, including Burundi, Iraq, the Philippines, and Ukraine, among others. While, Cuba has the largest decrease of IHD attributable to diet low in fiber, with AAPC of -9.53% (95%CI: -9.66%, -9.39%) for DALY rate and − 8.26% (95%CI: -8.43%, -8.08%) for death rate (Table S1 ).

The IHD burden attributable to diet low in fiber in different countries and territories in 2019

The burden of IHD attributable to diet low in fiber in regions with different SDI

In 2019, The age-standardized DALY and death rates (per 100,000 population) of IHD resulting from were highest in Low-middle SDI region (165.40,95%UI: 74.95,266.36 and 7.11,95%UI: 3.23,11.37), while the minimum estimates were in high SDI region (53.58, 95%UI: 20.43,89.00 and 2.93, 95% UI: 1.16,4.78) (Table  1 ). There were none significant correlations between SDI and DALY ( r =-0.01, P  = 0.833) and death ( r =-0.06, P  = 0.375) rates of IHD resulting from diet low in fiber burden (Fig S2 ). Between 1990 and 2019, all the five SDI regions showing a downward trend of burden of IHD resulting from diet low in fiber, however, from High SDI to low SDI, the degree of decline progressive reduction (Fig.  1 ).

This study offers a comprehensive evaluation of the global impact of IHD stemming from a diet deficient in fiber. As per our knowledge, this marks the inaugural research to delve into this matter, yielding several noteworthy insights that demand the attention of health policymakers. This study underscores a substantial global burden of IHD resulting from a fiber-deficient diet, affecting a significant populace. Specifically, in 2019, diet deficient in fiber accounted for a notable share of IHD-related fatalities (3.82%) and DALY (4.36%), exhibiting significant geographical disparities. Furthermore, we discerned a concerning upward trajectory in the number of IHD-related deaths and DALY attributed to a fiber-deficient diet globally. These disclosures possess profound implications for policymakers, especially in the global pursuit to address the obstacles stemming from IHD.

Globally, dietary fiber consumption remains insufficient. Numerous nations recommend 25–35 g of dietary fiber daily for adults. Yet, in the United States from 2011 to 2012, men averaged 20.5 g daily, while women consumed 16.2 g. Similarly, in Canada in 2011, men averaged 16.5 g, and women 14.3 g. In the United Kingdom, from 2009 to 2012, men consumed an average of 14.7 g, while women averaged 12.8 g [ 15 ]. In Asia, Japanese individuals consumed between 15 and 20 g daily in the 1980s and 1990s [ 16 ]. In comparison, China had a relatively higher intake in 2011, with 19.4 g for men and 17.6 g for women [ 17 ]. Therefore, to address this IHD burden stemming from low-fiber diets, it is highly necessary to comprehensively analyze the global distribution of the burden of IHD associated with insufficient dietary fiber intake.

Our research indicates that the diet low in fiber associated IHD burden is more significant among males and individuals of advanced age. This disparity may stem from the tendency of males and younger adults towards consuming less nutritious dietary choices [ 18 ], as well as the delayed impact of dietary intake on health outcomes, ultimately leading to an elevated risk of developing IHD [ 19 ]. Additionally, there is often a lack of comprehension among males and older individuals regarding the interconnection between dietary intake and overall health [ 20 ]. Also, the burden for females were lower, potentially stemming from a strong correlation with estrogen levels prior to menopause, as estrogens are known to exhibit antioxidant and antiapoptotic effects on cardiomyocytes during ischemic conditions [ 21 ]. Consequently, to alleviate the burden of IHD, it’s crucial to prioritize early nutritional interventions (such as health education) targeting young males and adopt effective plans for older males.

Across regions, geographical disparities played a significant role in shaping the epidemiological patterns of IHD resulting from a diet low in fiber. Our analysis revealed that regions like South Asia, Central Asia, Southeast Asia (including countries e.g., Mongolia, Afghanistan, Tajikistan, Uzbekistan and Yemen) have exhibited higher rates of IHD resulting from dietary in low fiber. The primary cause of this disparity lies in socioeconomic disparities and the uneven spread of dietary factors among diverse regions. This can be evidenced by our findings that high SDI region has the minimum burden estimates. Those residing in high-SDI areas often exhibit healthier dietary patterns, preferring to consume foods that are nutritionally beneficial like whole grains and fruits, in comparison to those residing in lower-SDI regions [ 22 , 23 , 24 ]. A study in China also found that dietary fiber intake increased among people in highly urbanized communities, while the opposite trend was observed in low-urbanization areas [ 17 ], suggesting that socioeconomic imbalances and uneven distribution may influence dietary habits. Furthermore, data gathered from 52 nations revealed that urban areas experiencing an upsurge in income levels consume greater quantities of fruits and vegetables [ 25 ]. Besides, individuals residing in low- and middle-income regions might be unaware of the positive health impacts of fiber intake, coupled with their constrained access to fresh food markets stemming from transportation limitations [ 26 , 27 ]. Additionally, numerous low-SDI countries prioritize exporting fruits and vegetables rich in dietary fiber instead of consuming them locally, contributing significantly to an increased risk of exposure to a low-fiber diet [ 28 ]. Furthermore, additional research is crucial to identify the underlying factors that contribute to the region-level heterogeneity in the IHD burden resulting from diet in low fibers.

Between 1990 and 2019, we observed that most regions displayed a downward trend of the burden of IHD attributable to diet low in fiber, except for Central Sub-Saharan Africa and Southern Sub-Saharan Africa. In sub-Saharan Africa, food prices tend to be relatively high, while dietary quality lags behind [ 29 ]. Moreover, in specific nations and their neighboring regions, both domestic and international tensions persist, which have significantly hampered food production and trade, thus contributing to poor dietary quality [ 30 ]. It’s noteworthy that the global consumption of dietary fiber is currently suboptimal. To alleviate the disease burden resulting from low-fiber diet in various regions, comprehensive interventions are imperative, particularly in low-SDI regions. For instance,

utilizing mass media, educational initiatives and the adoption of favorable food pricing policies can effectively promote dietary fiber consumption by enhancing public knowledge of healthy dietary practices [ 31 , 32 ]. It is imperative to devise public health strategies tailored to the dietary patterns and disease burdens in diverse regions.

The interpretation of our research is subject to certain constraints. Firstly, our estimations heavily relied on the availability of data. Although nationwide censuses and surveys furnish valuable data on IHD mortality, the scope and reliability of such information is still constrained, particularly in remote and economically deprived areas, thereby posing challenges to the precision of burden assessments. Secondly, when assessing the magnitude of the effect of the correlation between a fiber-deficient diet and IHD in the GBD 2019 study, it might be subject to potential confounding factors, and interactions among dietary components. As a global epidemiological analysis, such as missing data, inconsistency, and large methodological variation between data sources in different countries may also introduce bias to the results. Thirdly, for countries with large territorial areas, such as China and the United States, we have not fully analyzed the burden of IHD related to insufficient dietary fiber within their regions. A more refined analysis of disease burden at a geographical scale could help formulate better public health policies.

Conclusions

Our research underscores the pressing global concern of significantly rising cases of IHD attributed to diet in low fiber, highlighting the urgent need for health policymakers to take swift action and intervene. Moreover, our research highlights specific regions burdened with heavy disease rates, alongside vulnerable groups that necessitate increased attention and appropriate resources. Fundamentally, our discoveries provide crucial perspectives that can contribute towards formulating public health policies designed to alleviate and adapt to the health implications of a low-fiber diet.

Data availability

The datasets used and/or analysed during the current study available from the corresponding author on reasonable request.

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Acknowledgements

We highly appreciate the work by the GBD 2019 collaborators.

This research was funded by grants from the Humanities and Social Science Project of Anhui Provincial Education Department (SK2021A0433) and Science and Technology projects of Bengbu Medical College 2020 (2020byzd168).

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Conceptualization, N.W. and L.X.; methodology, N.W.; software, N.W.; validation, L.X. and L.W.; formal analysis, N.W.; investigation, N.W.; resources, N.W.; data curation, L.W.; writ-ing—original draft preparation, N.W.; writing—review and editing, L.W.; visualization, N.W.; supervision, B.T., Y.H. and L.X.; project administration, L.X.; funding acquisition, L.X. and B.T. All authors have read and agreed to the published version of the manuscript.

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Wei, N., Wang, L., Tang, B. et al. A global analysis of the burden of ischemic heart disease attributable to diet low in fiber between 1990 and 2019. BMC Cardiovasc Disord 24 , 491 (2024). https://doi.org/10.1186/s12872-024-04156-8

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Dynamic trends of ischemic heart disease mortality attributable to high low-density lipoprotein cholesterol: a joinpoint analysis and age-period-cohort analysis with predictions

Affiliations.

• 1 Department of Cardiology, Shanxi Provincial People's Hospital, Fifth Hospital of Shanxi Medical University, Taiyuan, Shanxi, 030012, China.
• 2 Department of Cardiology, The First People's Hospital of Jinzhong, Jinzhong, 030602, China.
• 3 School of Foreign Languages, Yantai University, Yantai, Shandong, 264005, China.
• 4 Department of Cardiology, Wenshui People's Hospital, Wenshui, Shanxi, 032100, China.
• 5 Medical Department, Shanghai Ashermed Medical Technology Co., Ltd, Shanghai, 200030, China. [email protected].
• PMID: 39261844
• PMCID: PMC11389117
• DOI: 10.1186/s12944-024-02274-y

Aims: The purpose of this study was to analyze the dynamic trends of ischemic heart disease (IHD) mortality attributable to high low-density lipoprotein cholesterol (LDL-C).

Methods: Data on IHD mortality attributable to high LDL-C from 1990 to 2021 were extracted from the global disease burden database. Joinpoint software was used to estimate the average annual percentage change (AAPC) in the age-standardized mortality rate (ASMR). An age‒period‒cohort model was used to analyze the impacts of age, period, and cohort on these changes. The Bayesian framework was used to predict IHD mortality attributable to high LDL-C from 2022 to 2040.

Results: The overall ASMR of IHD attributable to high LDL-C decreased from 50. 479 per 100,000 people in 1990 to 32.286 per 100,000 people in 2021, and ASMR of IHD attributable to high LDL-C was higher in males than in females. The longitudinal age curves of the overall IHD mortality attributable to high LDL-C showed a monotonic upward trend, especially after 65 years of age. The period and cohort effect relative risk (RR) values of overall IHD mortality attributable to high LDL-C showed a downward trend. The overall ASMR of IHD attributable to high LDL-C is predicted to show a downward trend, and male IHD mortality attributable to high LDL-C is expected to be higher than that of females.

Conclusion: This study revealed a sustained decrease in IHD mortality attributable to high LDL-C over three decades, with a continued decline expected. Despite this, gender disparities persist, with males experiencing higher mortality rates and elderly individuals remaining a vulnerable group.

Keywords: Age-period-cohort analysis; High low-density lipoprotein cholesterol; Ischemic heart disease; Joinpoint analysis; Prediction analysis.

© 2024. The Author(s).

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Conflict of interest statement

The authors declare no competing interests.

Trends in the number of…

Trends in the number of deaths and the ASMR per 100,000 people for…

Joinpoint trend of the ASMR…

Joinpoint trend of the ASMR for IHD attributable to high LDL-C from 1990–2021.…

Age-period-cohort analysis of IHD mortality…

Age-period-cohort analysis of IHD mortality attributable to high LDL-C from 1990–2021. Local drift…

Prediction of the ASMR and…

Prediction of the ASMR and number of deaths in IHD attributable to high…

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Coronary artery disease.

Rai Dilawar Shahjehan ; Beenish S. Bhutta .

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Last Update: August 17, 2023 .

• Continuing Education Activity

Coronary artery disease is a common heart condition that involves atherosclerotic plaque formation in the vessel lumen. This leads to impairment in blood flow and thus oxygen delivery to the myocardium. It is a cause of major morbidity and mortality in the US and worldwide. To avoid the high morbidity and mortality associated with this condition, it must be promptly diagnosed and treated. This activity illustrates the evaluation, diagnosis, and management of coronary artery disease and highlights the role of the healthcare team in evaluating and treating patients with this condition.

• Identify the etiology of coronary artery disease.
• Outline the evaluation of coronary artery disease.
• Discuss the management options available for coronary artery disease.
• Introduction

Coronary artery disease is a condition in which there is an inadequate supply of blood and oxygen to the myocardium. It results from occlusion of the coronary arteries and results in a demand-supply mismatch of oxygen. It typically involves the formation of plaques in the lumen of coronary arteries that impede blood flow. It is the major cause of death in the US and worldwide. At the beginning of the 20th century, it was an uncommon cause of death. Deaths due to CAD peaked in the mid-1960s and then decreased however, it still is the leading cause of death worldwide. [1]

Coronary artery disease is a multifactorial phenomenon. Etiologic factors can be broadly categorized into non-modifiable and modifiable factors. Non-modifiable factors include gender, age, family history, and genetics. Modifiable risk factors include smoking, obesity, lipid levels, and psychosocial variables. In the Western world, a faster-paced lifestyle has led people to eat more fast foods and unhealthy meals which has led to an increased prevalence of ischemic heart diseases. In the US, better primary care in the middle and higher socioeconomic groups has pushed the incidence towards the later part of life. Smoking remains the number one cause of cardiovascular diseases. In 2016, the prevalence of smoking among the United States among adults was found to be at 15.5 %. [2]  

The male gender is more predisposed than the female gender. Hypercholesterolemia remains an important modifiable risk factor for CAD. Increased low-density lipoproteins (LDL) increased the risk for CAD and elevated high-density lipoproteins (HDL) decrease the incidence of CAD. An individual's 10-year risk of atherosclerotic cardiovascular disease can be calculated using the ASCVD equation available online on the American Heart Association portal. Markers of inflammation are also strong risk factors for coronary artery disease. High sensitivity CRP (hsCRP) is thought to be the best predictor of coronary artery disease in some studies although uses for it in a practical setting are controversial. [3]

• Epidemiology

Coronary artery disease is very common in both developed and developing worlds. In one study, it was estimated that CAD represented 2.2% of the overall global burden of disease and 32.7% of cardiovascular diseases. It costs over 200 billion dollars annually to the health care system in the United States. It is estimated that 7.6% of men and 5.0% of women in the US lived with coronary artery disease from 2009 to 2012 based on the national health survey done by the American Heart Association (AHA). This amount to 15.5 million Americans afflicted with the disease during this time. [4] [5]  

The incidence of CAD is observed to rise with age, regardless of gender. In the ONACI registry in France, the incidence of CAD was about 1% in the 45 to 65 age group, which increased to about 4% as the age group reached 75 to 84 years. [6]

• Pathophysiology

The hallmark of the pathophysiology of CAD is the development of atherosclerotic plaque. Plaque is a build-up of fatty material that narrows the vessel lumen and impedes the blood flow. The first step in the process is the formation of a "fatty streak." Fatty streak is formed by subendothelial deposition of lipid-laden macrophages, also called foam cells. When a vascular insult occurs, the intima layer breaks, and monocytes migrate into the subendothelial space where they become macrophages. These macrophages take up oxidized low-density lipoprotein (LDL) particles, and foam cells are formed. T cells get activated, which releases cytokines only to aid in the pathologic process. Growth factors released activate smooth muscles, which also take up oxidized LDL particles and collagen and deposit along with activated macrophages and increase the population of foam cells. This process leads to the formation of subendothelial plaque.

Over time, this plaque could grow in size or become stable if no further insult occurs to the endothelium. If it becomes stable, a fibrous cap will form, and the lesion will become calcified over time. As time passes, the lesion can become hemodynamically significant enough that not enough blood would reach the myocardial tissue at the time of increased demands, and angina symptoms would occur. However, symptoms would abate at rest as the oxygen requirement comes down. For a lesion to cause angina at rest, it must be at least 90% stenosed. Some plaques can rupture and lead to exposure of tissue factor, which culminates in thrombosis. This thrombosis could cause subtotal or total occlusion of the lumen and could result in the development of acute coronary syndrome (ACS) in the form of unstable angina, NSTEMI, or STEMI, depending on the level of insult. [7]

Classification of coronary artery disease is typically done as under:

• Stable ischemic heart disease (SIHD)
• ST-elevation MI (STEMI)
• Non-ST elevation MI (NSTEMI)
• Unstable angina
• History and Physical

It is very important to take a detailed history and physical examination before proceeding towards further workup. Coronary artery disease could manifest as stable ischemic heart disease (SIHD) or acute coronary syndrome (ACS). It can further progress into congestive heart failure (CHF) if not controlled. Patients should be asked about chest pain, its relation to physical activity, and radiation of the pain into the jaw, neck, left arm, or into the back. Dyspnea should be evaluated for rest and also on activity. The patient should also be asked about syncope, palpitations, tachypnea, lower extremity edema, orthopnea, and exercise capacity. A family history of ischemic heart diseases should be obtained along with dietary, smoking, and lifestyle habits.

Physical examination should include inspection, palpation, and auscultation. One should inspect for any acute distress, jugular venous distention, and peripheral edema. In palpation, one should palpate for fluid thrill and heave. The extent of peripheral edema if present should be evaluated. The distension of the jugular vein should be measured. In auscultation, the heart should be auscultated in all four locations and lungs should also be auscultated with a special focus on the lower zones.

There are several modalities to evaluate for coronary artery disease including EKG, Echo, CXR, Stress test, cardiac catheterization, and blood work to name the main ones. These tests are done depending on the context in which patients are presenting. The following are details on different diagnostic modalities we have available for the evaluation of coronary artery disease:

Electrocardiogram (EKG) 

EKG is a very basic yet enormously helpful test in the evaluation of coronary artery disease. It measures electrical activity in the cardiac conduction system and is measured by 10 leads attached to the skin at standardized locations. It provides information about both the physiology and anatomy of the heart. It typically has 12 leads on the paper that is printed once the test is performed and each lead correlates with the specific location of the heart. Important information to notice on an EKG is a heart's rate, rhythm, and axis. After that, information regarding acute and chronic pathologic processes can be obtained. In acute coronary syndrome, one can see ST-segment changes and T wave changes. If an ACS has degenerated into arrhythmias, that can also be seen. In chronic settings, EKG can show information like axis deviation, bundle branch blocks, and ventricular hypertrophy. EKG is also a cost-effective and readily available testing modality that is not user-dependent. 

Echocardiography

Echocardiography is an ultrasound of the heart. It is a useful and non-invasive mode of testing that is performed in both acute and chronic and inpatient and outpatient settings. In acute settings, it could tell about wall motion, valvular regurgitation and stenosis, infective or autoimmune lesions, and chamber sizes. It also is useful in the diagnosis of acute pulmonary pathologies like pulmonary embolism. It also evaluates the pericardial cavity. In chronic settings, it can be done to see the same information mentioned above and also a response to the therapy. It also is used in an outpatient setting as part of stress testing. In addition to diagnostics, it also has a role in therapeutics for example, pericardiocentesis could be performed with the needle-guided by echocardiography. This test is user-dependent and could be costly compared to EKG. [8]

Stress Test

The stress test is a relatively non-invasive test to evaluate for coronary artery disease. It is used in the setting of suspected angina or angina equivalent and is helpful in ruling in or out coronary pathology when interpreted in an appropriate setting. During the test, the heart is artificially exposed to stress and if the patient gets certain abnormal EKG changes in ST segments or gets symptoms of angina, the test is aborted at that point and coronary artery disease is diagnosed. EKGs are obtained before, during, and after the procedure, and the patient is continuously monitored for any symptoms. There are mainly two types of stress tests; exercise stress test and pharmacologic stress test. In exercise stress tests, the patient has to run on a treadmill until he achieves 85% of the age-predicted maximal heart rate. If a patient develops exertional hypotension, hypertension (>200/110 mmHg), ST-segment elevations or depression, or ventricular or supraventricular arrhythmias. [9]

Chest X-ray

Chest X-ray is an important component of the initial evaluation of cardiac disease. The standard imaging films include standing posteroanterior (PA) and left lateral decubitus. Sometimes, anteroposterior (AP) projection is obtained especially in inpatient settings with the patient lying down, however, this interpretation of AP films is significantly limited. Proper analysis of PA and AP views provides useful and cost-effective information about the heart, lungs, and vasculature. Interpretation should be done in a stepwise pattern so that important information is not overlooked. 

Blood work aids in establishing the diagnosis and assessing therapeutic responses. In acute settings, cardiac enzymes and B-type natriuretic peptides are often done along with complete blood counts and metabolic panels. BNP provides information about volume overload of cardiogenic origin however it has its limitations. It can be falsely elevated in kidney diseases and falsely low in obesity. Cardiac enzymes like CK and troponin provide information about an acute ischemic event. In chronic settings, lipid panel provides important prognostic information. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) aid in assessing disease like acute pericarditis. Liver function tests (LFT) can be done to evaluate for an infiltrative process that can affect the liver and heart simultaneously like hemochromatosis. Liver tests are also done to assess increased right heart pressures, especially in chronic settings.

Cardiac Catheterization

Cardiac catheterization is the gold standard and most accurate modality to evaluate ischemic coronary heart disease. It is however an invasive procedure with associated complications. Not everyone is a candidate for the procedure. In non ACS settings, patients with intermediate pretest probability for CAD are usually the right candidates for it. In the ACS setting, all STEMI patients and selected NSTEMI patients get an emergent cardiac catheterization. This procedure is done in a cardiac catheterization lab, is expertise dependent, and is done under moderate sedation. There is contrast exposure in the procedure which could cause serious allergic reactions and kidney injury.

• Treatment / Management

Coronary artery disease could present either as stable ischemic heart disease (SIHD) or acute coronary syndrome (ACS). The former present in a chronic setting while the latter presents more in an acute setting. The management depends on the particular disease type. We will discuss the management of each subtype separately: 

Stable Ischemic Heart Disease

Stable ischemic heart disease presents as stable angina. Stable angina typically presents as substernal chest pain or pressure that worsens with exertion or emotional stress and gets relieved with rest or nitroglycerin and is of 2 months duration. It is important to know that classic anginal symptoms could be absent and it could present differently with atypical symptoms and exertional dyspnea instead in certain demographic groups including women, elderly age, and diabetics. Management of SIHD includes both non-pharmacologic and pharmacologic interventions. Lifestyle modifications include smoking cessation, regular exercise, weight loss, good control of diabetes and hypertension, and a healthy diet. Pharmacologic interventions include cardioprotective and antianginal medications.

Every patient should get guideline-directed medical therapy (GDMT) which includes low dose aspirin, beta-blocker, as-needed nitroglycerin, and moderate to high-intensity statin. If symptoms are not controlled with this, beta-blocker therapy should be titrated up to heart rates 55-60, and the addition of calcium channel blocker and long-acting nitrates should be considered. [10]  Ranolazine could also be added to relieve refractory anginal symptoms. If maximal GDMT has failed to relive angina, cardiac catheterization should be done to visualize the coronary anatomy and a decision should be made for percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) based on the patient profile. [11]

Acute Coronary Syndrome

The acute coronary syndrome presents as sudden onset substernal chest pain or pressure typically radiating to the neck and left arm and may be accompanied by dyspnea, palpitations, dizziness, syncope, cardiac arrest, or new-onset congestive heart failure. Prompt EKG is necessary for all patients with ACS to assess for STEMI and typically is done pre-hospital by an emergency medical services crew. STEMI is recognized by the presence of ST elevation in contiguous leads of 1 mm in limb leads or precordial leads excepting V2 and V3. In V2 and V3, men need to have 2 mm elevations and women 1.5 mm to qualify for STEMI diagnosis. New-onset left bundle branch block (LBBB) is also considered a STEMI equivalent. If STEMI is present, emergency PCI is warranted in a PCI capable facility or if a PCI facility is available within 2 hours distance. If the PCI capable facility is more than 2 hours away, intravenous thrombolytic therapy is indicated after making sure there are no contraindications to it.

It is important to differentiate a true STEMI from other conditions that mimic STEMI on EKG like acute pericarditis, Brugada syndrome, early repolarization changes, and LVH associated changes. All patients should get a full dose of sublingual aspirin (324 mg) upon presentation. Nitrates should be given for pain relief after making sure there are no contraindications to nitrates like hypotension, RV failure, and consumption of phosphodiesterase inhibitors in the past 24-48 hours. High-dose statin therapy and beta-blockers should also be initiated early. P2Y12 inhibitors (prasugrel, ticagrelor, or prasugrel) should be started based on the patient profile. Patients who have NSTE ACS should get anticoagulation, typically heparin or enoxaparin are used. For NSTEMI, early invasive therapy within 24 hours is advised for patients with intermediate to high TIMI scores (>2). [12] [13]

Regular visits with cardiologists and family physicians are key to good long term management of coronary artery disease. Medication adherence and lifestyle modification are important.

• Differential Diagnosis

Coronary artery disease has a wide range of differential diagnoses because of the proximity of the heart with adjacent organs, including the lungs, stomach, big vessels, and musculoskeletal organs. Acute anginal chest pain could mimic acute pericarditis, myocarditis, prinzmetal angina, pericardial effusion, acute bronchitis, pneumonia, pleuritis, pleural effusion, aortic dissection, GERD, peptic ulcer disease, esophageal motility disorders, and costochondritis. Stable ischemic heart disease could also mimic GERD, Peptic ulcer disease, costochondritis, and pleuritis. History, physical examination, and diagnostic studies should be carefully carried out to narrow down the differential diagnosis and reach an accurate diagnosis.

• Toxicity and Adverse Effect Management

Both medical and surgical management for ischemic heart disease is associated with their side effects and complications. These undesirable effects could be mitigated by careful selection, physician expertise, and patient education. Aspirin therapy is associated with bleeding, idiosyncratic, and allergic drug reactions. [14]  Statin therapy can cause myalgias, diarrhea, and arthralgias among side effects. [15]  

Beta-blockers could cause bradycardia and hypotension. ACEIs could result in hypotension, dizziness, creatinine elevation, cough, and allergic reactions including angioedema. [16]  PCI can possibly cause coronary artery perforation, stent thrombosis in an acute setting, and in-stent restenosis on chronic basis. [17] CABG can have its own complications including but not limited to arrhythmias, cardiac tamponade, post-op bleeding, infection, renal impairment, and phrenic nerve injury.

The prognosis of the disease depends on multiple factors some of which could be modified while others are non-modifiable. Patient's age, gender, family history and genetics, ethnicity, dietary and smoking habits, medication compliance, availability of healthcare and financial status, and the number of arteries involved are some of the factors. Comorbid conditions including diabetes mellitus, hypertension, dyslipidemia, and chronic kidney disease also have a role in the overall outcome. [18]

• Complications

Arrhythmias, acute coronary syndrome, congestive heart failure, mitral regurgitation, ventricular free wall rupture, pericarditis, aneurysm formation, and mural thrombi are the main complication associated with coronary artery disease. [19] [20] [10]

• Deterrence and Patient Education

Coronary artery disease is caused by a combination of modifiable and nonmodifiable factors. Primary care providers should focus on the modifiable risk factor modification on each routine visit. Tight control of diabetes, hypertension and lipid levels in addition to smoking cessation, weight loss and exercise can make a huge difference. Since it is a global public health concern, in school curriculums and different avenues of media, more awareness needs to be created. 

• Pearls and Other Issues

Several landmark trials were done over the past few decades which have totally changed the way we care for coronary artery disease patients. It is beyond the scope of this article to discuss individual trial results, however, the following are the names of some important studies. ISIS-2, CURE, CLARITY-TIMI 28, TIRTON-TIMI 38, PLATO, and CURRENT-OASIS 7 trials were done regarding guidelines for antiplatelet medications. [21]  SYNERGY, ACUITY, ExTRACT-TIMI 25, OASIS-5, and ATLAS ACS/ TIMI 52 were done about the use of anticoagulation. ADMIRAL, ACUITY, ISAR-REACT 3, and HORIZONS-AMI are famous trials regarding GpIIb/IIIa use, COMMIT for beta-blockers while SHOCK, DANAMI-2, BASKET-LATE, TIMACS, and BASKET-PROVE are about PCI and CABG. MIRACL trial was done about statin use.

• Enhancing Healthcare Team Outcomes

Evaluation of ischemic heart disease can frequently present a diagnostic dilemma. Such patients can present non-specific symptoms like chest pain or shortness of breath. The cause of chest pain or shortness of breath could be due to a myriad of diseases including gastrointestinal, cardiac, musculoskeletal, psychological, and pulmonary causes. While a cardiologist is often involved as a central player, it is important to take other team members on board as indicated including a gastroenterologist, pulmonologist, and psychiatrist. Radiologists also are an important resource in the whole process. Nurses are a very important part of the diagnostic and therapeutic workup as well as they provide key bedside information not witnessed by the physicians in their short encounters.

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Classification of CAD. Image created by the author Rai Dilawar Shahjehan, MD.

Disclosure: Rai Dilawar Shahjehan declares no relevant financial relationships with ineligible companies.

Disclosure: Beenish Bhutta declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Shahjehan RD, Bhutta BS. Coronary Artery Disease. [Updated 2023 Aug 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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