Publications by authors named "Ashok Talreja"

Background: Doppler echocardiography (DE), chest radiography (CXR), serum B-type natriuretic peptide (BNP) measurement and physical examination are all commonly employed to estimate left ventricular diastolic pressure (LVDP) in clinical care. There are no published studies directly comparing the diagnostic accuracy of these tests.

Methods And Results: DE, BNP, CXR, and physical examination were performed on 56 consecutive patients immediately following clinically indicated cardiac catheterization with measurement of LVDP.

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Background: Atrial fibrillation (Afib) that occurs after a successful atrial flutter (AFL) ablation may negate the potential benefits of the ablation. Afib occurs more often when severe left ventricular systolic dysfunction (LVSD) is present. We hypothesized that even after a successful AFL ablation, the incidence of postablation Afib is increased when severe LVSD is present.

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The recrudescence of interest in manipulation of the arginine vasopressin system and especially of V2 vasopressin receptor blockade in heart failure stems from the limited efficacy and possible detrimental effects of loop diuretics. The "braking phenomenon," hypertrophy of the collecting duct cells, and altered pharmacodynamics contribute to loop diuretic resistance in heart failure. Selective (tolvaptan) and nonselective (conivaptan) V2 vasopressin receptor antagonists now known as "vaptans" promote free-water excretion that is labeled aquaresis and correct hyponatremia in patients with severe heart failure.

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Data regarding the effects of beta blockers on left ventricular (LV) function after 12 months are scarce in ischemic and nonischemic cardiomyopathy. Echocardiograms of 72 patients with ischemic and nonischemic cardiomyopathy, who were free of clinical events susceptible to alter LV function while receiving carvedilol or metoprolol for at least 24 months, were prospectively reanalyzed. Twelve months after beta-blocker initiation, LV ejection fraction (EF) increased by > or = 5% in 75% of patients, whereas EF failed to increase by 5% or decreased in the remaining 25%.

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A number of large randomized, placebo-controlled mortality trials provided evidence-based data to guide the treatment of patients with systolic heart failure, but, with one exception, similar trials in patients with diastolic heart failure (DHF) either are not yet completed or have not been conducted at all. However, randomized outcomes trials conducted in patients with hypertension with and without left ventricular hypertrophy and in patients with vascular diseases at high risk for cardiovascular events provide a strong rationale for long-term angiotensin-converting enzyme inhibition or angiotensin receptor blockade in patients with DHF. The treatment of patients with acutely decompensated DHF remains purely empirical.

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Background: Vascular endothelial functions, other than nitric oxide (NO)-mediated control of vasomotor tone, are poorly characterized in patients with chronic heart failure (CHF). Veins and arteries are exposed to the same circulating proinflammatory mediators in patients with CHF. The present study tested whether endothelial cell activation occurs in veins of patients with decompensated CHF and whether activation, if present, subsides with return to a clinically compensated state.

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The rationale behind the use of angiotensin-converting enzyme (ACE) inhibitors has evolved considerably since their approval for the treatment of hypertension. The initial rationale behind their use for the treatment of chronic heart failure was to duplicate with one agent the hemodynamic effects produced by the hydralazine-isosorbide dinitrate combination, i.e.

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Limited availability of endothelial tissue is a major constraint when investigating the cellular mechanisms of endothelial dysfunction in patients with metabolic and cardiovascular diseases. We propose a novel approach that combines collection of 200-1,000 endothelial cells from a superficial forearm vein or the radial artery, with reliable measurements of protein expression by quantitative immunofluorescence analysis. This method was validated against immunoblot analysis in cultured endothelial cells.

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