A Non-atherosclerotic Heart Tears Apart: A Case of Spontaneous Coronary Artery Dissection in a Healthy Postmenopausal Woman.

Due to limited understanding and knowledge of spontaneous coronary artery dissection (SCAD), it is typically believed to affect young peripartum women. We present a case of a post-menopausal older woman who suffered an acute non-ST segment elevation myocardial infarction (NSTEMI), secondary to a SCAD of the right posterior descending artery (PDA), after strenuous exercise. As the patient was hemodynamically stable and without signs of ongoing ischemia, she was managed conservatively. SCAD should be in differentials for patients presenting with acute coronary syndrome (ACS) who have no or few cardiovascular atherosclerotic risk factors. SCAD can be missed due to low suspicion of ACS in young and healthy patients. ACS from SCAD is often misdiagnosed and/or mismanaged as atherosclerotic ACS. Increasing awareness about this condition can lead to earlier diagnosis and prevention of sudden cardiac deaths. As most cases of SCAD can be managed conservatively, differentiating it from atherosclerotic ACS can reduce unnecessary reperfusion procedures and complications thereof.

A Rare Case of Restrictive Cardiomyopathy Presenting With Large, Recurrent Pericardial Effusions.

The association between large pericardial effusion and restrictive cardiomyopathy (RCM) is uncommon and has seldom been described. We describe an uncommon case of a 31-year-old male with RCM who presented with large, recurrent pericardial effusion, heart failure, and echocardiographic findings showing progressive worsening of diastolic function even after total pericardiectomy who was eventually transferred for cardiac transplant evaluation.

A Case of Recurrent Coronary Subclavian Steal Syndrome.

Coronary subclavian steal syndrome (CSSS) is one of the rare complications of coronary artery bypass graft surgery (CABG). This phenomenon is a potential complication after left internal mammary artery (LIMA) to left anterior descending artery (LAD) CABG. A proximal stenosis of the left subclavian artery (SA) could cause retrograde flow from LIMA to left SA, which characterizes the mechanism of CSSS. We describe a unique case of recurrent CSSS in a 64-year-old female who presented with one month of exertional dyspnea and acute onset chest pain. She had an extensive coronary artery disease history with CABG 15 years prior to presentation and CSSS treated with left SA stent placement nine years later. She also underwent percutaneous intervention with stents placed in the saphenous vein graft. Although electrocardiogram, cardiac enzymes, and stress test did not show any evidence of acute ischemic changes, perfusion scan detected large areas of partially reversible ischemia. Cardiac catheterization was performed, which showed in-stent restenosis of the left SA and retrograde flow from the LIMA to the left SA indicative of recurrence of CSSS. Left SA arteriogram confirmed in-stent restenosis of the left SA, which was treated with balloon angioplasty and stent placement.

Reciprocal ST-Segment Changes in Myocardial Infarction: Ischemia at Distance Versus Mirror Reflection of ST-Elevation.

BACKGROUND: Reciprocal ST-depression in the electrocardiograms (ECGs) of patients with ST-elevation myocardial infarction (STEMI) results from either true ischemia at a distance via collateral circulation diverting blood to the infarcted region or an electrical phenomenon that results from a mirror reflection of ST-elevation. We aimed to identify the role of reciprocal ECG changes in predicting collateral circulation to the infarcted area determined angiographically. METHODS: In a retrospective study, ECG and angiography of 53 STEMI patients admitted to SUNY Upstate Medical University in 2014 were reviewed independently by experts blinded to the results of ECG and coronary angiography. RESULTS: Reciprocal changes (RC) in ECG were present in 41 patients (77%) and on angiography, 14 patients (26%) exhibited collateral vessels to the ischemic areas. No correlation was found between the presence of RC and collateral circulation (P = 0.384), or between the depth of reciprocal ST-depression and the degree of the collateral circulation (P = 0.195). However, 84% of patients without collaterals exhibited resolution of RC after successful percutaneous coronary intervention (PCI) (P = 0.036), suggesting that the ST depressions that resolved after reperfusion were directly caused by the culprit vessel. Patients without RC presented late after symptom onset (9.25 versus 3.83 hours, P = 0.004), also suggesting time related resolution. CONCLUSIONS: RC had no relation to or predictive value for collaterals on angiography. Among late presenting patients, RC were less frequent. Thus, reciprocal ST-depression may represent subendocardial ischemia from the primary coronary event or simply an electrical phenomenon, rather than ischemia at distance from impaired collateral circulation.

Kounis syndrome: A review article on epidemiology, diagnostic findings, management and complications of allergic acute coronary syndrome.

Kounis syndrome (KS) is a hypersensitivity coronary disorder induced by exposure to drugs, food, environmental and other triggers. Vasospastic allergic angina, allergic myocardial infarction (MI) and stent thrombosis with occluding thrombus infiltrated by eosinophils and/or mast cells constitute the three main variants of this syndrome. We reviewed 175 patients who fulfilled the definition of one of the three types of KS. The epidemiology, diagnostic findings, management and complications were reviewed in this article.

Renal Denervation in Heart Failure: A New Therapeutic Paradigm.

Heart failure constitutes a significant source of morbidity and mortality in the United States, and its incidence and prevalence continue to grow, increasing its burden on the health care system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This complex interaction is characterized by a pathophysiological disequilibrium between the heart and the kidney, in which cardiac malfunction promotes renal impairment, which in turn feeds back, resulting in further deterioration of cardiovascular function. Multiple neurohumoral and hemodynamic mechanisms are involved in this cardiorenal dyshomeostasis, including resistance to compensatory cardiac natriuretic peptides, leading to sodium retention, volume overload, and organ remodeling. Previous studies in animal models of heart failure have demonstrated that renal denervation promotes a robust natriuresis and diuresis as well as increased response of endogenous and exogenous natriuretic agents. With the recent development of minimally invasive renal denervation in humans, it is possible to suggest that this technique may become effective and important in the management of renal sodium and water metabolism in heart failure.

Revascularization in Severe Left Ventricular Dysfunction: Does Myocardial Viability Even Matter?

Left ventricular dysfunction is a powerful prognostic predictor in patients with coronary artery disease and increasing number of patients with CAD and ischemic left ventricular (LV) dysfunction is a major clinical problem. Congestive heart failure is a frequent complication which is associated with significant health care costs and two-third of cases have ischemic cardiomyopathy. In such patients, coronary revascularization can lead to symptomatic and prognostic improvement and reversal of LV remodeling which led to the concept of viable myocardium to select patients in whom recovery of LV function and improvement of prognosis will outweigh the risk of surgical revascularization. The aim of this review article is to understand the different modalities for assessing myocardial viability and clinical impact of revascularization in relation to the evidence of viability in patients with LV dysfunction.

Cardiac troponins: bench to bedside interpretation in cardiac disease.

Cardiac troponins are the preferred biomarkers for the determination of acute myocardial necrosis. The high sensitivity of the available assays has significantly increased the detection of microscopic amounts of myocardial damage. Although compelling evidence indicates that elevated cardiac troponins are markers of poor prognosis and increased mortality, irrespective of the clinical scenario, small elevations can be seen in protean conditions and may confound the diagnosis of acute coronary syndromes. Emerging evidence suggests multiple different cellular mechanisms leading to cardiac troponin release, which challenge long held paradigms such as equivalency between troponin release into the circulation and irreversible cell death. Hence, knowledge of the physiology and pathophysiology of these cardiac biomarkers is essential for their accurate interpretation and consequent correct clinical diagnosis. Herein, the current relevant information about cardiac troponins is discussed, with special emphasis on pathophysiology and clinical correlates.

The kidney in heart failure: friend or foe?

Heart failure constitutes a significant source of morbidity and mortality in the United States and its incidence and prevalence continue to grow, increasing its burden on the health care system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This complex interaction is characterized by a pathophysiological disequilibrium between the heart and the kidney, in which cardiac malfunction promotes renal impairment, which in turn feeds back for further deterioration of cardiovascular function. Multiple neurohumoral and hemodynamic mechanisms are involved in this cardiorenal dyshomeostasis, including the deficiency of and/or resistance to compensatory natriuretic peptides, leading to sodium retention, volume overload and organ remodeling. Management of patients with cardiorenal dysfunction can be challenging and should be individualized. Emerging therapies must address the impairment of both organs to secure better clinical outcomes. To this end, a multidisciplinary approach is warranted to achieve optimal results.

Vascular endothelial dysfunction in patients with newly diagnosed type 2 diabetes and effects of 2-year and 5-year multifactorial intervention.

OBJECTIVES: Investigate short- and long-term effect of multifactorial intervention on endothelial dysfunction in patients with newly diagnosed type 2 diabetes. BACKGROUND: Whether multifactorial intervention reduces cardiovascular risk in type 2 diabetes is largely controversial, partially because of lack of reliable method for endothelial dysfunction detection. Using high-resolution ultrasonographical flow-mediated vasodilatation (FMD), we completed a 5-year randomized prospective intervention trial in patients with newly diagnosed type 2 diabetes. We have studied the effect of multifactorial intervention therapy on their endothelial dysfunction. METHODS: One hundred eight patients with newly diagnosed type 2 diabetes, and 83 healthy subjects received measurement of brachial artery FMD and endothelium-independent dilatation (EID). Diabetic patients were assigned into four groups, treated with: (A) hypoglycemic and antihypertensive agents, (B) hypoglycemic, antihypertensive and lipid-lowering agents, (C) hypoglycemic, antihypertensive and lipid-lowering agents, and vitamin E, and (D) hypoglycemic, antihypertensive and lipid-lowering agents, and compound salvia tablets. Both FMD and EID were remeasured after 24- and 60-month treatment. RESULTS: FMD in diabetic patients was significantly lower than those in healthy subjects. After 24-month treatment, there was no FMD change. However, FMD improved significantly after 60-month treatment. The differences between 24- and 60-month are also significant. EID did not change significantly after both 24- and 60-month treatments. CONCLUSIONS: (1) FMD-detectable endothelial dysfunction exists in newly diagnosed type 2 diabetic patients. (2) Reverse of endothelial function occurs only after long-term (60-month) multifactorial intervention. (3) FMD could potentially help early identification, stratification, and treatment of endothelial dysfunction in type 2 diabetic patients.

El síndrome cardiorenal en insuficiencia cardíaca: un paradigma en evolución / The cardiorenal syndrome in heart failure: an envolving paradigm

Background: Heart failure constitutes a significant source of morbidity and mortality in the United States and its incidence and prevalence continue to grow, increasing its burden on the health care system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This interaction, termed the cardiorenal syndrome, is a complex phenomenon characterized by a pathophysiological disequilibrium between the heart and the kidney, in which malfunction of one organ subsequently promotes the impairment of the other. Multiple neuro-humoral mechanisms are involved in this cardiorenal interaction, including the deficiency of and/or resistance to compensatory natriuretic peptides, leading to sodium retention, volume overload and organ remodeling. Management of patients with the cardiorenal syndrome can be challenging and should be individualized. Emerging therapies must address the function of both organs in order to secure better clinical outcomes. To this end, a multidisciplinary approach is recommended to achieve optimal results.

The cardiorenal syndrome in heart failure: an evolving paradigm.

Heart failure constitutes a significant source of morbidity and mortality in the United States, and its incidence and prevalence continue to grow, increasing its burden on the healthcare system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This interaction, termed the cardiorenal syndrome, is a complex phenomenon characterized by a pathophysiologic disequilibrium between the heart and the kidney, in which malfunction of 1 organ consequently promotes the impairment of the other. Multiple neurohumoral mechanisms are involved in this cardiorenal interaction, including the deficiency of and/or resistance to compensatory natriuretic peptides, leading to sodium retention, volume overload and organ remodeling. Management of patients with the cardiorenal syndrome can be challenging and should be individualized. Emerging therapies must address the function of both organs to secure better clinical outcomes. To this end, a multidisciplinary approach is recommended to achieve optimal results.

Takotsubo cardiomyopathy: a case report.

A 57-year-old Caucasian woman presented to the emergency department with chest discomfort after testifying in a child custody battle in court. Electrocardiography (ECG) revealed ST-segment elevation in the lateral leads, and T-wave inversions in the inferior and lateral leads. The creatine kinase, creatine kinase-MB, and troponin I concentrations were elevated on presentation. Despite the ECG changes and elevated cardiac markers, coronary angiography demonstrated normal arteries. Left ventricular angiogram revealed an aneurysm at the apex. Takotsubo cardiomyopathy was diagnosed on the basis of these characteristic findings. The patient was discharged on her third hospital day without any complications from the coronary angiography.