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Although it is well known that incessant atrial tachyarrhythmias can cause left ventricular (LV) dysfunction, little is known about focal atrial tachycardia and LV dysfunction.
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After acute coronary syndromes (ACS), re-currence of ischemia is a harbinger of worse prognosis.
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New markers for a variety of diseases have recently received considerable attention, specifically B-type natriuretic peptide (BNP), N-terminal-pro-BNP, C-reactive protein, or CRP, and CRP-hs (high sensitivity). Levels of these compounds are useful guides in assessing the severity of important medical conditions, such as congestive heart failure and acute myocardial infarction chest pain.
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Syncope is commonly accepted to be a danger sign in patients with hypertrophic cardiomyopathy (HCM). In this paper, Spirito et al report data from a registry of 1,511 patients with HCM who have been followed longitudinally at four institutions.
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It has been postulated that angiotensin-converting enzyme (ACE) inhibitors and angiotensin II-receptor blockers (ARBs) decrease the risk of developing atrial fibrillation both indirectly by better control of hypertension and heart failure and directly by effects on fibrosis,
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NSAIDs in the elderly; managing GI and CVD risk with NSAIDs; low-dose naltrexone and fibromyalgia; treating glucocorticoid-induced bone loss; FDA Actions.
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Patients presenting to the emergency department (ED) with acute chest pain are a significant portion of our health care budget. Current recommendations for the assessment and management of these patients involve extended periods of observation for repeated biomarkers and electrocardiograms (ECG). This often results in hospital admission to "rule out" myocardial infarction. Any advance in the speed or accuracy of diagnosis of the cause of chest pain, or to rule out myocardial ischemia as the cause, would be a significant clinical advance.
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Dr. George Dourgas presented the results of the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS AMI) analysis of predictors of stent thrombosis in more than 3,600 patients, and showed that higher doses of clopidogrel (600 mg) pharmacologic therapy, lesion characteristics, and the length of stents were predictors of early-stent thrombosis.
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The introduction of drug-eluting stents (DES) was met with enthusiasm from the interventional cardiology community because of the dramatic reduction in rates of in-stent restenosis (ISR). However, it came to be recognized that this clinical benefit, due to reduced proliferation of smooth muscle cells, came at a price.
