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PubMed2005

The less familiar side of heart failure: symptomatic diastolic dysfunction.

Arrange for echocardiography or radionuclide angiography within 72 hours of a heart failure exacerbation. An ejection fraction >50% in the presence of signs and symptoms of heart failure makes the diagnosis of diastolic heart failure probable. To treat associated hypertension, use angiotensin receptor blockers (ARBs), angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, calcium channel blockers, or diuretics to achieve a blood pressure goal of <130/80 mm Hg. When using beta-blockers to control heart rate, titrate doses more aggressively than would be done for systolic failure, to reach a goal of 60 to 70 bpm. Use ACE inhibitors/ARBs to decrease hospitalizations, decrease symptoms, and prevent left ventricular remodeling.

Adrenergic beta-Antagonists↗
PubMed2001

Left ventricular diastolic dysfunction during demand ischemia: rigor underlies increased stiffness without calcium-mediated tension. Amelioration by glycolytic substrate.

OBJECTIVES: The goal of this study was to determine the subcellular mechanism(s) underlying increased left ventricular (LV) diastolic chamber stiffness (DCS) during angina (demand ischemia). BACKGROUND: Increased DCS may result from increased diastolic myocyte calcium concentration and/or rigor. Therefore, we assessed the effects of direct alterations of both calcium-activated tension and high-energy phosphates on increased DCS. METHODS: Demand ischemia was reproduced in isolated, isovolumic, red-cell perfused rabbit hearts by imposing low-flow ischemia and pacing tachycardia. This resulted in increased DCS. Interventions were performed after LV end-diastolic pressure had increased approximately 7 mm Hg. Initially, to determine the effects of altered calcium concentration or myofilament calcium responsiveness, hearts received either: 1) 5 or 14 mmol/L calcium chloride; 2) 8 mmol/L egtazic acid; 3) 5 mmol/L butane-dione-monoxime (BDM); or 4) 50 mmol/L ammonium chloride (NH4Cl). Then, to assess the contribution of decreased high-energy phosphate supply, hearts received 5) glucose (25 mmol/L) and insulin (400 microU/ml). RESULTS: 1) Calcium chloride, 5 and 14 mmol/L, increased LV systolic pressure by 42% and 70%, respectively (p < 0.001), indicating increased calcium-activated tension, but did not further increase DCS, implying intact diastolic calcium resequestration. 2) Egtazic acid reduced LV systolic pressure by 30% (p < 0.001), indicating reduced intracellular calcium, but failed to reduce increased DCS. 3) Butane-dione-monoxime and NH4Cl chloride affected contractile function (i.e., a calcium-driven force) but did not alter increased DCS. 4) Glucose and insulin, which increase high-energy phosphates during ischemia, reduced increased DCS by 50% (p < 0.001). CONCLUSIONS: Increased DCS during demand ischemia was insensitive to maneuvers altering intracellular calcium concentration or myofilament calcium-responsiveness, that is, evidence against an etiology of calcium-activated tension. In contrast, increased glycolytic substrate ameliorated increased DCS, supporting a primary mechanism of rigor-bond formation.

Angina Pectoris↗
PubMed1994

Mechanism of the diastolic dysfunction induced by glycolytic inhibition. Does adenosine triphosphate derived from glycolysis play a favored role in cellular Ca2+ homeostasis in ferret myocardium?

Several lines of evidence indicate that glycolysis is especially important for normal diastolic relaxation and for the maintenance of cellular ion homeostasis in myocardium. To elucidate whether the glycolytic flux of ATP contributes to diastolic tone and to the regulation of intracellular Ca2+, myocardial content of sugar phosphates ([SP]) and intracellular Ca2+ concentration ([Ca2+]i) were measured in isolated, perfused ferret hearts using nuclear magnetic resonance. Glucose and acetate were used as substrates for glycolysis and oxidative phosphorylation, respectively. Glycogen was effectively depleted after 15-min perfusion with glucagon (2 mg/liter), as verified by the lack of rise in [SP] during exposure to iodoacetate (100 microM) in substrate-free perfusate. Despite the fact that glycolytic flux had been blocked both by iodoacetate and by absence of substrate, end-diastolic left ventricular pressure (EDP) remained unchanged (P > 0.15, n = 6). The subsequent addition of glucose to the perfusate led to SP accumulation and a marked rise in EDP, with a significant correlation between EDP and [SP] (r = 0.86 +/- 0.04, P < 0.01, n = 6). A similar correlation was observed when glucose in the perfusate was replaced by 2-deoxyglucose (r = 0.78 +/- 0.09, P < 0.01, n = 3). Fluorine nuclear magnetic resonance measurements of [Ca2+]i verified that EDP faithfully reports changes in diastolic [Ca2+]i under the present experimental conditions. Thus, intracellular Ca2+ overload is caused by the accumulation of SP rather than by the inhibition of glycolysis per se. Glycolysis may appear to be important because its by-products are deleterious, and not necessarily because glycolytically derived ATP plays a favored role in ion homeostasis.

Adenosine Triphosphate↗
PubMed2002

Left ventricular hypertrophy and diastolic dysfunction in healthy pregnant women.

OBJECTIVE: The purpose of this study was to examine which hemodynamic parameters change under the natural volume overload of pregnancy. STUDY DESIGN: 46 healthy pregnant women were echocardiographically examined during the course of pregnancy. To evaluate left ventricular diastolic function, mitral inflow and pulmonary venous flow profiles were used. Fractional shortening and left ventricular muscle mass were calculated. RESULTS: In the course of pregnancy the left ventricular muscle mass index increased (from 66 +/- 6 to 96 +/- 9 g/m(2)), fractional shortening decreased (from 38 +/- 4 to 32 +/- 6%) and a disturbed diastolic relaxation pattern was documented. Eight weeks after delivery, all left ventricular systolic and diastolic functional parameters returned to normal values. CONCLUSION: The natural volume overload in pregnancy leads to a reversible 'physiological' left ventricular hypertrophy, a short-term decrease in systolic function and a significant change in left ventricular diastolic function.

Adult↗