Current cardiology reports
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The search for the ideal therapy for valve replacement continues. The major options include mechanical or tissue valves, with an increasing variety of tissue valves becoming available. The key factor continues to be thrombogenicity versus durability. ⋯ Mitral valve surgery has greater potential for repair, which affords preservation of the native valve, optimizing function and reducing long-term complications. An increasingly popular concept is treatment of secondary or functional mitral valve regurgitation in the setting of depressed left ventricular function. The routine use of intraoperative transesophageal echocardiography and a trend toward the use of minimally invasive procedures are altering the conduct of valve operations.
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Observational studies have established a strong association between the presence of patent foramen ovale (PFO) and increased risk of ischemic stroke. The mechanism involved is presumed to be a paradoxical embolism from a venous thrombus that travels via the PFO to the systemic circulation. The best treatment modality to prevent recurrent stroke in patients with PFO remains undefined. ⋯ The Patent Foramen Ovale in Cryptogenic Stroke Study has demonstrated that antiplatelet and anticoagulant therapies are of equal benefit in preventing recurrent neurologic events in stroke patients with a PFO. Medical therapy should remain as the initial choice of secondary prophylactic therapy. PFO closure, either surgical or percutaneous, may further reduce event rates; however, this remains to be demonstrated because no randomized trial to date has compared PFO closure with medical therapy.
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Radiofrequency ablation is a valuable adjunctive therapy to implantable defibrillators in patients with recurrent monomorphic ventricular tachycardia (VT) after myocardial infarction. Episodes of VT are markedly reduced in most patients, and the major complications are less than 5%. ⋯ Epicardial mapping and ablation are needed in some patients. Continued advances in technology can be expected to further improve results.
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Vasodilatory edema, a common adverse effect of antihypertensive therapy with vasodilators, is related to several mechanisms, including arteriolar dilatation (causing an increase in intracapillary pressure), stimulation of the renin-angiotensin-aldosterone system, and fluid volume retention. Vasodilatory edema is dose-dependent and most common with direct arteriolar dilators such as minoxidil or hydralazine, and in decreasing order of frequency with the dihydropyridine calcium antagonists, a-blockers, antiadrenergic drugs, and nondihydropyridine calcium antagonists. Not all dihydropyridine calcium antagonists are created equal with regard to vasodilatory edema. ⋯ The addition of an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) to a dihydropyridine calcium antagonist significantly reduces vasodilatory edema. In contrast, the addition of a diuretic has little effect on vasodilatory edema. Thus, low-dose combination therapy (of a dihydropyridine calcium antagonist with either an ACE inhibitor or an ARB) may be preferred over high-dose monotherapy.