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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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Chapter 5:  10 Real Cases on Acute Heart Failure Syndrome: Diagnosis, Management, and Follow-Up

Swathi Roy; Gayathri Kamalakkannan

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Case review, case discussion.

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Case 1: Diagnosis and Management of New-Onset Heart Failure With Reduced Ejection Fraction

A 54-year-old woman presented to the telemetry floor with shortness of breath (SOB) for 4 months that progressed to an extent that she was unable to perform daily activities. She also used 3 pillows to sleep and often woke up from sleep due to difficulty catching her breath. Her medical history included hypertension, dyslipidemia, diabetes mellitus, and history of triple bypass surgery 4 years ago. Her current home medications included aspirin, atorvastatin, amlodipine, and metformin. No significant social or family history was noted. Her vital signs were stable. Physical examination showed bilateral diffuse crackles in lungs, elevated jugular venous pressure, and 2+ pitting lower extremity edema. ECG showed normal sinus rhythm with left ventricular hypertrophy. Chest x-ray showed vascular congestion. Laboratory results showed a pro-B-type natriuretic peptide (pro-BNP) level of 874 pg/mL and troponin level of 0.22 ng/mL. Thyroid panel was normal. An echocardiogram demonstrated systolic dysfunction, mild mitral regurgitation, a dilated left atrium, and an ejection fraction (EF) of 33%. How would you manage this case?

In this case, a patient with known history of coronary artery disease presented with worsening of shortness of breath with lower extremity edema and jugular venous distension along with crackles in the lung. The sign and symptoms along with labs and imaging findings point to diagnosis of heart failure with reduced EF (HFrEF). She should be treated with diuretics and guideline-directed medical therapy for congestive heart failure (CHF). Telemetry monitoring for arrythmia should be performed, especially with structural heart disease. Electrolyte and urine output monitoring should be continued.

In the initial evaluation of patients who present with signs and symptoms of heart failure, pro-BNP level measurement may be used as both a diagnostic and prognostic tool. Based on left ventricular EF (LVEF), heart failure is classified into heart failure with preserved EF (HFpEF) if LVEF is >50%, HFrEF if LVEF is <40%, and heart failure with mid-range EF (HFmEF) if LVEF is 40% to 50%. All patients with symptomatic heart failure should be started on an angiotensin-converting enzyme (ACE) inhibitor (or angiotensin receptor blocker if ACE inhibitor is not tolerated) and β-blocker, as appropriate. In addition, in patients with New York Heart Association functional classes II through IV, an aldosterone antagonist should be prescribed. In African American patients, hydralazine and nitrates should be added. Recent recommendations also recommend starting an angiotensin receptor-neprilysin inhibitor (ARNI) in patients who are symptomatic on ACE inhibitors.

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A case report of myocardial infarction with non-obstructive coronary artery disease: Graves’ disease-induced coronary artery vasospasm

Margo klomp.

y1 Department of Cardiology, Dijklander Hospital, Location Hoorn, Maelsonstraat 3, 1624 NP Hoorn, the Netherlands

Sarah E Siegelaar

y2 Department of Endocrinology and Metabolism, Amsterdam University Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands

Tim P van de Hoef

y3 Department of Cardiology, Amsterdam University Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands

Marcel A M Beijk

Associated data.

Coronary artery spasm can occur either in response to drugs or toxins. This response may result in hyper-reactivity of vascular smooth muscles or may occur spontaneously as a result of disorders in the coronary vasomotor tone. Hyperthyroidism is associated with coronary artery spasm.

Case summary

A 49-year-old female patient with a 2-day history of intermittent chest pain and electrocardiographic evidence of myocardial ischaemia was referred for emergency coronary angiography. This revealed severe right coronary artery (RCA) and left main (LM) coronary artery ostial vasospasm, both subsequently relieved with administration of multiple doses intracoronary nitroglycerine. Intravascular optical coherence tomography showed absence of atherosclerosis and no evidence of thrombus or dissection confirming the diagnosis of coronary artery vasospasm. Laboratory tests of the thyroid function were performed immediately after coronary angiography revealing Graves’ disease as the cause of vasospasm.

Our case represents a rare presentation of Graves’ disease-induced RCA and LM coronary artery ostial vasospasm. In patients with coronary artery vasospasm thyroid function study should be mandatory, especially in young female patients.

Learning points

• Coronary artery spasm can be induced by a hyperactive thyroid.
• When angiography demonstrates spontaneous severe multivessel coronary artery vasospasm, the presence of a systemic condition as underlying cause should be considered.
• In patients with coronary artery spasm thyroid function study should be mandatory, especially for the young female patients.

Introduction

Myocardial infarction in the absence of obstructive (>50% stenosis) coronary artery disease (MINOCA) is found in approximately 6% of all patients with acute myocardial infarction (MI) who are referred for coronary angiography. 1 , 2 The term MINOCA should be reserved for patients in whom there is an ischaemic basis for their clinical presentation and should be considered a ‘working diagnosis’. There are a variety of causes that can result in MINOCA and it is important that patients are appropriately diagnosed so that specific therapies to treat the underlying cause can be prescribed when possible. Thus, in the evaluation of patients presenting with clinical evidence of MI and a rise or fall in cardiac biomarkers but absence of obstructive coronary artery disease (CAD) at coronary angiography, it is important to exclude (i) overt causes for the elevated troponin (e.g. sepsis, pulmonary embolism), (ii) overlooked obstructive disease (e.g. occlusion of a small coronary artery subsegment resulting from plaque disruption or embolism), and (iii) subtle non-ischaemic mechanisms of myocyte injury that can mimic MI (e.g. myocarditis). 3 Once abovementioned causes are excluded by use of available diagnostic resources, a diagnosis of MINOCA can be made.

There are disparate aetiologies causing MINOCA and they can be grouped into 2 :

• Atherosclerotic causes of myocardial necrosis (i.e. secondary to epicardial coronary artery disorders), such as atherosclerotic plaque rupture, ulceration, fissuring, erosion, or coronary dissection with non-obstructive or no CAD [MI Type 1 according to the ‘Fourth Universal Definition of Myocardial Infarction’ (2018)]. 4
• Non-atherosclerotic causes of myocardial necrosis (i.e. imbalance between oxygen supply and demand), such as epicardial coronary artery spasm, coronary microvessel dysfunction, coronary embolism/thrombosis, spontaneous coronary artery dissection, or systemic conditions resulting in supply-demand mismatch (e.g. tachyarrhythmias, anaemia, hypotension, thyrotoxicosis) [MI Type 2 according to the ‘Fourth Universal Definition of Myocardial Infarction’ (2018)].

We report a case of MINOCA with a rare underlying cause resulting in severe right coronary artery (RCA) and the left main (LM) ostial vasospasm.

Case presentation

A 49-year-old previously healthy Caucasian woman presented to the emergency cardiac care department of a local hospital with a 2-day history of intermittent retrosternal chest pain. Since 2 h the pain worsened and she developed shortness of breath, nausea, and severe sweating. She was an active smoker and had a negative familial history for cardiovascular disease. She was not taking any regular medication and had no history of drug abuse. Physical examination documented a blood pressure of 185/92 mmHg, heart rate of 112 b.p.m., respiratory rate 25 per minute, and temperature 37.9°C. Heart sounds were normal on auscultation with no audible murmur. The rest of the clinical examination was unremarkable. The electrocardiogram showed a sinus tachycardia with widespread ST-segment depression in the inferior leads and leads V 4 –V 6 with inverted T waves and ST-segment elevation in lead aVR and V 1 ( Figure 1 ). Assuming an MI, a loading dose of aspirin 300 mg and ticagrelor 180 mg was administered and intravenous heparin 5000 IE was given. Moreover, metoprolol 2.5 mg intravenously was administered and nitroglycerine continuous infusion was started. Promptly, the patient was transferred to our hospital for emergency diagnostic coronary angiography. On arrival at the catheterization laboratory, the patient had continuous chest pain and her electrocardiogram (ECG) was unchanged. Coronary angiography revealed severe RCA and the LM ostial vasospasm ( Figure ​ Figure2 2 A and B , Supplementary material online, Movies S1 and S2 ), with dampening of the blood pressure tracings, both subsequently relieved with administration of multiple doses (200 µg/dose) intracoronary nitroglycerine ( Figure ​ Figure3 3 A and B , Supplementary material online, Movies S3 and S4 ). Intravascular optical coherence tomography (OCT) was performed showing both arteries without atherosclerosis, thrombus or dissection ( Figure ​ Figure3 3 C and D , Supplementary material online, Movies S5 and S6 ). Finally, left ventricular angiography showed no wall motion abnormalities ( Supplementary material online, Movie S7 ). The patient was free of symptoms when she left the catheterization laboratory and the ECG was normalized.

Admission electrocardiogram.

Coronary angiography showing severe right coronary artery (red arrow, A ) and left main ostial vasospasm (red arrow, B ).

Coronary angiography after administration of nitroglycerine of the right coronary artery ( A ) and left coronary artery ( B ) and intravascular optical coherence tomography of the right coronary artery ( C ) and left coronary artery ( D ) showing absence of atherosclerosis, thrombus, or dissection.

Further investigation revealed a Troponin T maximum of 0.451 µg/L (range 0–0.05 µg/L), N-terminal pro-B-type natriuretic peptide of 293 ng/L (range 0–249 ng/L), elevated serum free thyroxine of 59.9 pmol/L (range 12–22 pmol/L), suppressed thyroid-stimulating hormone (TSH) of <0.001 mE/L (range 0.5–5 mE/L), and elevated TSH receptor antibody of 20.2 E/L (range 0–1.8 E/L), confirming the diagnosis of Graves’ disease. Physical examination revealed a small nodule in the thyroid gland but no ophthalmological features. An thyroid ultrasound was not performed neither was a toxicology screen. The Burch–Wartofsky Point Scale (BWPS) score can predict the likelihood that biochemical thyrotoxicosis is thyroid storm. The BWPS is an empirically derived scoring system that takes into account the severities of symptoms of multiple organ decompensation, including thermoregulatory dysfunction, tachycardia/atrial fibrillation, disturbances of consciousness, congestive heart failure, and gastro-hepatic dysfunction, as well as the role of precipitating factors. A BWPS score of >45 represents a thyroid storm, between 25–45 an impending storm and <25 storm unlikely. Based on hyperthermia, tachycardia and gastrointestinal-hepatic dysfunction, the patients’ score was 25 indicated an impending thyroid storm. She was started on thiamazole 30 mg o.d. and within 1 day of treatment serum free thyroxine lowered from 59.9 pmol/L to 42.6 pmol/L. Therefore, iodine therapy or surgery was not considered necessary. Dual antiplatelet therapy was discontinued and a long-acting nitrate and a dihydropyridine calcium channel blocker was prescribed till euthyroidism was restored. At telephone follow-up 1 week after discharge, she was free of symptoms and she experienced no side effects of the medication. As she was a labour migrant, she returned to her home country shortly thereafter.

This report illustrates a case of multivessel coronary artery spasm secondary to Graves’ disease. In our case, the presence of ST depression ≥1 mm in six or more surface leads, coupled with ST-segment elevation in aVR and/or V1, suggested multivessel ischaemia or LM coronary artery obstruction. Emergent coronary angiography was performed and showed severe ostial vasospasm of the RCA. To exclude the possibility of catheter-induced vasospasm, the initial visualization of the left coronary artery was performed by a non-selective injection which clearly showed severe vasospasm of the ostium of the LM. This severe ostial vasospasm of the RCA and the LM only improved after administration of multiple doses of intracoronary nitroglycerine. Hereafter, we decided to perform an OCT to rule out an atherosclerotic cause of myocardial necrosis. Optical coherence tomography showed a normal vessel wall with a typical three-layer appearance visible in both coronary arteries. 5 Additional laboratory testing revealed hyperthyroidism as a cause of multivessel coronary artery spasm. Although several reports of hyperthyroidism-associated angina pectoris (secondary to coronary spasm) have appeared, to our knowledge, this is one of the few cases with angiographically documented multivessel coronary artery spasm and the first report describing the use of intracoronary imaging with OCT.

Graves thyrotoxicosis is an autoimmune disease and is the most common cause of thyrotoxicosis. It is known that hyperthyroidism can cause coronary artery spasm, in particular in patients with Graves’ disease as was the case in our patient. Multiple hypothetical pathophysiological pathways have been suggested for the mechanism of thyroid hormone-induced coronary artery spasm. Hyperthyroidism can lead to a hyperkinetic circulatory system with tachycardia, increased pulse pressure, and decreased peripheral resistance secondary to vasorelaxation. 6 Along with a hypersensitivity to vasoconstrictive agents, this general hypermetabolic state precipitates an imbalance between blood supply and oxygen demand during a thyrotoxic state. 7 The exaggerated vascular reactivity is secondary to an excessive endothelial nitric oxide production and enhanced sensitivity of the endothelial component which can lead to coronary artery spasm in some patients. 6 Controlling thyroid activity will alleviate symptoms and correct the vascular abnormalities without the need of invasive interventions. In our case, laboratory tests of the thyroid function were only performed immediately after coronary angiography. Invasive coronary vascular imaging (intravascular ultrasound or OCT) can help to discriminate between an atherosclerotic vs. non-atherosclerotic cause of myocardial necrosis. Moreover, in MINOCA patients left ventricular angiography, echocardiography, or cardiac magnetic resonance imaging can rule out takotsubo cardiomyopathy or other underlying causes when there is no evident vasospasm at coronary angiography.

In a review by Al Jaber et al . 8 evaluating hyperthyroidism-associated angina pectoris, it was shown that the age range of reported patients was 44–75 years, with female predominance, more commonly in Asian patients, and the time from symptom onset to diagnosis varied between days to 8 months. Moreover, hyperthyroid manifestations may be mild or absent. The pattern of cardiac presentation included angina pectoris, MI, cardiogenic shock, ventricular tachyarrythmias, cardiac arrest, and/or pulmonary oedema. Importantly, a review of coronary angiograms in patients with an overactive thyroid showed that the LM coronary artery was significantly more involved than the RCA. 9 Delay in diagnosis of hyperthyroidism-induced myocardial necrosis in these patients may result in complications and unnecessary interventions. With appropriate antithyroid therapy, the prognosis of patients with hyperthyroidism-associated angina pectoris is excellent. 9 , 10

Lead author biography

Margo Klomp, MD, PhD, MBA, is a General Cardiologist at the Dijklander Hospital in Noord-Holland, the Netherlands with specific interests in management.

Supplementary material

Supplementary material is available at European Heart Journal - Case Reports online.

Supplementary Material

Ytaa191_supplementary_data, acknowledgements.

Both authors received no funding in the development of this case report

Slide sets: A fully edited slide set detailing this case and suitable for local presentation is available online as Supplementary data .

Consent: The author/s confirm that written consent for submission and publication of this case report including image(s) andassociated text has been obtained from the patient in line with COPE guidance.

Conflict of interest: none declared.

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Cardiovascular disease case studies

Read international case studies of cardiovascular disease prevention in a joint report by the BHF and Public Health England.   

The UK has made progress on bringing down the premature death rate associated with cardiovascular disease (CVD) in recent years. But CVD still affects around seven million people in the UK, is responsible for one in five premature deaths and is estimated to cost the healthcare economy £9 billion each year.

To continue to make progress in preventing CVD, we can learn from other nations who have successfully delivered programmes that improve cardiovascular health.

In 2018, jointly with Public Health England, we commissioned a report identifying successful CVD prevention programmes from around the world, produced by public health consultancy group Solutions for Public Health.

The report, International Cardiovascular Disease Prevention case studies, outlines ten case studies that illustrate approaches that may be applicable and effective within the UK.

Download the report [PDF]

International context of CVD prevention

Ten case studies are detailed in the report, including:

• The COACH programme in Australia where trained nurses coach people who have, or are at high risk of developing, CVD over the phone
• Hypertension Canada, which aims to train healthcare professionals to diagnose hypertension and follow evidence-based guidelines on managing the condition
• The Million Hearts initiative in the US, which aims to align CVD prevention efforts across 50 states by focusing on a small set of evidence-based priorities such as controlling blood pressure and smoking cessation
• The CHAP initiative in Canada, where older people were encouraged to attend volunteer-run sessions to encourage them to become more aware of their cardiovascular risk
• The HONU project in the US, where people at risk of CVD were assigned a health coach to support lifestyle change, and initiatives were set up in workplaces and at community and government level to improve diet and activity levels

Alongside the case studies, the report also makes recommendations for how to implement effective CVD prevention programmes in the UK, and provides background on current CVD prevention programmes in England.

You can access the report now for the full details on these case studies and recommendations.

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Coronary heart disease as a case study in prevention: potential role of incentives

Affiliation.

• 1 Division of Cardiology, University of Vermont College of Medicine, University Health Center Campus, 1 S. Prospect St, Burlington, VT 05401, USA. [email protected]
• PMID: 22285317
• DOI: 10.1016/j.ypmed.2011.12.025

Coronary atherosclerosis is a complex entity with behavioral, genetic and environmental antecedents. Most risk factors for coronary heart disease have a behavioral component. These include tobacco use, hyperlipidemia, hypertension, obesity, insulin resistance, diabetes and physical inactivity. The role of monetary incentives to encourage healthful behaviors related to the prevention and treatment of coronary heart disease has received little attention. In this review, the potential role of monetary incentives to prevent or treat coronary heart disease is discussed. In particular, the potential role of providing incentives for patients to participate in cardiac rehabilitation (CR), a multi-risk intervention, is highlighted.

Copyright © 2011. Published by Elsevier Inc.

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• Potential benefits of weight loss in coronary heart disease. Ades PA, Savage PD. Ades PA, et al. Prog Cardiovasc Dis. 2014 Jan-Feb;56(4):448-56. doi: 10.1016/j.pcad.2013.09.009. Epub 2013 Oct 9. Prog Cardiovasc Dis. 2014. PMID: 24438737 Review.
• Impact of cardiac rehabilitation on metabolic syndrome in Iranian patients with coronary heart disease: the role of obesity. Kabir A, Sarrafzadegan N, Amini A, Aryan RS, Kerahroodi FH, Rabiei K, Taghipour HR, Moghimi M. Kabir A, et al. Rehabil Nurs. 2012 Mar-Apr;37(2):66-73. doi: 10.1002/RNJ.00012. Rehabil Nurs. 2012. PMID: 22434616
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Coronary Heart Disease

What are the coronary arteries.

Coronary arteries supply blood to the heart muscle. Like all other tissues in the body, the heart muscle needs oxygen-rich blood to function, and oxygen-depleted blood must be carried away. The coronary arteries run along the outside of the heart and have small branches that supply blood to the heart muscle.

What are the different coronary arteries?

The 2 main coronary arteries are the left main and right coronary arteries.

Left main coronary artery (LMCA). The left main coronary artery supplies blood to the left side of the heart muscle (the left ventricle and left atrium). The left main coronary artery divides into branches:

The left anterior descending artery branches off the left coronary artery and supplies blood to the front of the left side of the heart.

The circumflex artery branches off the left coronary artery and encircles the heart muscle. This artery supplies blood to the lateral side and back of the heart.

Right coronary artery (RCA). The right coronary artery supplies blood to the right ventricle, the right atrium, and the SA (sinoatrial) and AV (atrioventricular) nodes, which regulate the heart rhythm. The right coronary artery divides into smaller branches, including the right posterior descending artery and the acute marginal artery.

Additional smaller branches of the coronary arteries include the obtuse marginal (OM), septal perforator (SP), and diagonals.

Why are the coronary arteries important?

Since coronary arteries deliver blood to the heart muscle, any coronary artery disorder or disease can reduce the flow of oxygen and nutrients to the heart, which may lead to a heart attack and possibly death. Atherosclerosis is inflammation and a buildup of plaque in the inner lining of an artery causing it to narrow or become blocked. It is the most common cause of heart disease.

What is coronary artery disease?

Coronary heart disease, or coronary artery disease (CAD), is characterized by inflammation and the buildup of and fatty deposits along the innermost layer of the coronary arteries. The fatty deposits may develop in childhood and continue to thicken and enlarge throughout the life span. This thickening, called atherosclerosis, narrows the arteries and can decrease or block the flow of blood to the heart.

The American Heart Association estimates that over 16 million Americans suffer from coronary artery disease--the number one killer of both men and women in the U.S.

What are the risk factors for coronary artery disease?

Risk factors for CAD often include:

High LDL cholesterol , high triglycerides levels, and low HDL cholesterol

High blood pressure (hypertension)

Physical inactivity

High saturated fat diet

Family history

Controlling risk factors is the key to preventing illness and death from CAD.

What are the symptoms of coronary artery disease?

The symptoms of coronary heart disease will depend on the severity of the disease. Some people with CAD have no symptoms, some have episodes of mild chest pain or angina, and some have more severe chest pain.

If too little oxygenated blood reaches the heart, a person will experience chest pain called angina. When the blood supply is completely cut off, the result is a heart attack, and the heart muscle begins to die. Some people may have a heart attack and never recognize the symptoms. This is called a "silent" heart attack.

Symptoms of coronary artery disease include:

Heaviness, tightness, pressure, or pain in the chest behind the breastbone

Pain spreading to the arms, shoulders, jaw, neck, or back

Shortness of breath

Weakness and fatigue

How is coronary artery disease diagnosed?

In addition to a complete medical history and physical exam, tests for coronary artery disease may include the following:

Electrocardiogram (ECG or EKG). This test records the electrical activity of the heart, shows abnormal rhythms (arrhythmias), and detects heart muscle damage.

Stress test (also called treadmill or exercise ECG). This test is given while you walk on a treadmill to monitor the heart during exercise. Breathing and blood pressure rates are also monitored. A stress test may be used to detect coronary artery disease, or to determine safe levels of exercise after a heart attack or heart surgery. This can also be done while resting using special medicines that can synthetically place stress on the heart.

Cardiac catheterization . With this procedure, a wire is passed into the coronary arteries of the heart and X-rays are taken after a contrast agent is injected into an artery. It's done to locate the narrowing, blockages, and other problems.

Nuclear scanning. Radioactive material is injected into a vein and then is observed using a camera as it is taken up by the heart muscle. This indicates the healthy and damaged areas of the heart.

Treatment for coronary heart disease

Treatment may include:

Modification of risk factors. Risk factors that you can change include smoking, high cholesterol levels, high blood glucose levels, lack of exercise, poor dietary habits, being overweight, and high blood pressure.

Medicines. Medicine that may be used to treat coronary artery disease include:

Antiplatelets. These decrease blood clotting. Aspirin, clopidogrel, ticlopidine, and prasugrel are examples of antiplatelets.

Antihyperlipidemics. These lower lipids (fats) in the blood, particularly low density lipid (LDL) cholesterol. Statins are a group of cholesterol-lowering medicines, and include simvastatin, atorvastatin, and pravastatin, among others. Bile acid sequestrants--colesevelam, cholestyramine and colestipol--and nicotinic acid (niacin) are other medicines used to reduce cholesterol levels.

Antihypertensives. These lower blood pressure. Several different groups of medicines work in different ways to lower blood pressure.

Coronary angioplasty. With this procedure, a balloon is used to create a bigger opening in the vessel to increase blood flow. Although angioplasty is done in other blood vessels elsewhere in the body, percutaneous coronary intervention (PCI) refers to angioplasty in the coronary arteries to permit more blood flow into the heart. PCI is also called percutaneous transluminal coronary angioplasty (PTCA). There are several types of PCI procedures, including:

Balloon angioplasty. A small balloon is inflated inside the blocked artery to open the blocked area.

Coronary artery stent. A tiny mesh coil is expanded inside the blocked artery to open the blocked area and is left in place to keep the artery open.

Atherectomy. The blocked area inside the artery is cut away by a tiny device on the end of a catheter.

Laser angioplasty. A laser used to "vaporize" the blockage in the artery.

Coronary artery bypass . Most commonly referred to as simply "bypass surgery" or CABG (pronounced "cabbage"), this surgery is often done in people who have chest pain (angina) and coronary artery disease. During the surgery, a bypass is created by grafting a piece of a vein above and below the blocked area of a coronary artery, enabling blood to flow around the blockage. Veins are usually taken from the leg, but arteries from the chest or arm may also be used to create a bypass graft. Sometimes, multiple bypasses may be needed to fully restore blood flow to all regions of the heart.

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Coronary artery aneurysms: a clinical case report and literature review supporting therapeutic choices.

1. Introduction

1.1. definition and classification of coronary artery aneurysms, 1.2. risk factors, 1.3. clinical presentation, 1.4. diagnostic skills, 1.5. treatment, 1.6. caas in kawasaki disease, 2. clinical case presentation, 2.1. medical history, 2.2. examinations, 2.3. management, 3. conclusions, author contributions, conflicts of interest.

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Sannino, M.; Nicolai, M.; Infusino, F.; Giulio, L.; Usai, T.L.; Biscotti, G.; Azzarri, A.; De Angelis D’Ossat, M.; Calcagno, S.; Calcagno, S. Coronary Artery Aneurysms: A Clinical Case Report and Literature Review Supporting Therapeutic Choices. J. Clin. Med. 2024 , 13 , 5348. https://doi.org/10.3390/jcm13185348

Sannino M, Nicolai M, Infusino F, Giulio L, Usai TL, Biscotti G, Azzarri A, De Angelis D’Ossat M, Calcagno S, Calcagno S. Coronary Artery Aneurysms: A Clinical Case Report and Literature Review Supporting Therapeutic Choices. Journal of Clinical Medicine . 2024; 13(18):5348. https://doi.org/10.3390/jcm13185348

Sannino, Michele, Matteo Nicolai, Fabio Infusino, Luciani Giulio, Tommaso Leo Usai, Giovanni Biscotti, Alessandro Azzarri, Marina De Angelis D’Ossat, Sergio Calcagno, and Simone Calcagno. 2024. "Coronary Artery Aneurysms: A Clinical Case Report and Literature Review Supporting Therapeutic Choices" Journal of Clinical Medicine 13, no. 18: 5348. https://doi.org/10.3390/jcm13185348

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