Left ventricle diastolic dysfunction in diabetes: an update.
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Diabetes mellitus, a disease that has been reaching epidemic proportions, is an important risk factor to the development of cardiovascular complication. Diabetes causes changes within the cardiac structure and function, even in the absence of atherosclerotic disease. The left ventricular diastolic dysfunction (VE) represents the earliest pre-clinical manifestation of diabetic cardiomyopathy, preceding the systolic dysfunction and being able to evolve to symptomatic heart failure. The doppler echocardiography has emerged as an important noninvasive diagnostic tool, providing reliable data in the stages of diastolic function, as well as for systolic function. With the advent of recent echocardiographic techniques, such as tissue Doppler and color M-mode, the accuracy in identifying the moderate diastolic dysfunction, the pseudonormal pattern, has significantly improved. Due to cardio-metabolic repercussions of DM, a detailed evaluation of cardiovascular function in diabetic patients is important, and some alterations may be seen even in patients with gestational diabetes. (+info)
Characterization of left ventricular filling abnormalities and its relation to elevated plasma brain natriuretic peptide level in acute to chronic diastolic heart failure.
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BACKGROUND: Although Doppler left ventricular (LV) filling abnormalities have been extensively analyzed in patients with systolic heart failure (SHF), they have not yet been well characterized in patients with acute to chronic diastolic heart failure (DHF) in the light of plasma brain natriuretic peptide (BNP) levels. METHODS AND RESULTS: In 25 patients presenting with acute DHF and 25 with acute SHF, echo Doppler parameters and plasma BNP levels were obtained on admission and in the chronic stage. The mitral E/A ratio was lower in DHF patients than in SHF patients in the acute stage (1.3 +/-0.4 vs 1.8+/-0.9, p<0.05), and in the chronic stage of DHF the ratio decreased with plasma BNP level, but plasma BNP level was still greater than 100 pg/ml in 15 patients (60%). Among patients with DHF the plasma BNP level did not correlate with the mitral E/A ratio or deceleration time (r=0,25, p=NS; r=0,23, p=NS), but did with estimated pulmonary artery systolic pressure (r=0.64, p<0.01). CONCLUSIONS: A restrictive mitral flow velocity pattern is observed in only 25% of patients with DHF, so it is particularly important to recognize pseudonormalization in those with possible DHF. Persistently elevated plasma BNP level is not primarily caused by LV diastolic dysfunction, but by secondary alteration for hemodynamic adjustment (elevated LV end-diastolic pressure) in patients with DHF. (+info)
Novel mechanism and role of angiotensin II induced vascular endothelial injury in hypertensive diastolic heart failure.
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OBJECTIVE: The mechanism and role of angiotensin II-induced vascular endothelial injury is unclear. We examined the molecular mechanism of angiotensin (AII)-induced vascular endothelial injury and its significance for hypertensive diastolic heart failure. METHODS AND RESULTS: We compared the effect of valsartan and amlodipine on Dahl salt-sensitive hypertensive rats (DS rats). Valsartan improved vascular endothelial dysfunction of DS rats more than amlodipine, by inhibiting endothelial apoptosis and eNOS uncoupling more. Moreover, valsartan inhibited vascular apoptosis signal-regulating kinase 1 (ASK1) more than amlodipine. Thus, AT1 receptor contributed to vascular endothelial apoptosis, eNOS uncoupling, and ASK1 activation of DS rats. Using ASK1(-/-) mice, we examined the causative role of ASK1 in endothelial apoptosis and eNOS uncoupling. AII infusion in wild-type mice markedly caused vascular endothelial apoptosis and eNOS uncoupling accompanied by vascular endothelial dysfunction, whereas these effects of AII were absent in ASK1(-/-) mice. Therefore, ASK1 participated in AII-induced vascular endothelial apoptosis and eNOS uncoupling. Using tetrahydrobiopterin, we found that eNOS uncoupling was involved in vascular endothelial dysfunction in DS rats with established diastolic heart failure. CONCLUSIONS: AII-induced vascular endothelial apoptosis and eNOS uncoupling were mediated by ASK1 and contributed to vascular injury in diastolic heart failure of salt-sensitive hypertension. (+info)
Left ventricular untwisting rate by speckle tracking echocardiography.
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BACKGROUND: Recent studies validated the measurement of left ventricular (LV) untwisting rate (UR) by speckle tracking echocardiography. A few reports suggest that it may provide additional noninvasive insight into LV diastolic function. METHODS AND RESULTS: Simultaneous echocardiographic imaging and LV pressure measurements (7F Millar catheters) were performed in 8 adult dogs. Loading conditions were altered by caval occlusion, whereas lusitropic state was changed by dobutamine and esmolol infusion. Inferior vena cava occlusion at all experimental stages (baseline, dobutamine, esmolol) led to a significant decrease (P < or = 0.01) in LV end-systolic volume (ESV) and a significant increase in UR (P = 0.03). The best relation was observed between LV UR and ESV (r = -0.8, P < 0.001). The clinical study was conducted in 67 patients (age 57+/-17 years, 19 women) undergoing simultaneous right heart catheterization and echocardiographic imaging, with 20 healthy subjects as a control group. There were 34 patients with ejection fraction (EF) <50% (25+/-9%), and 33 patients with normal EF and diastolic dysfunction (64+/-7%). Patients with LV systolic dysfunction had a significantly lower UR (-55 omicron/s) in comparison with the control group (-89 omicron/s) and patients with normal EF (-104 omicron/s, P < 0.05), and the determinants of LV UR were twist, ESV, and tau (r2 = 0.83, P < 0.001). In patients with diastolic dysfunction and normal EF, twist and ESV were the independent predictors (r2 = 0.71, P < 0.001). CONCLUSIONS: LV UR is reduced in patients with depressed EF, but not in those with diastolic dysfunction and normal EF, and is primarily determined by twist and ESV. (+info)
C-reactive protein, diastolic dysfunction, and risk of heart failure in patients with coronary disease: Heart and Soul Study.
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BACKGROUND: High-sensitivity C-reactive protein (CRP) is an inflammatory marker that predicts coronary heart disease (CHD) and, in recent studies, incident heart failure (HF). Whether the association of inflammation with incident HF is explained by worse baseline left ventricular dysfunction or by underlying CHD is unknown. METHODS AND RESULTS: Serum CRP was measured in a cohort of 985 outpatients with established CHD from the Heart and Soul Study. During 3 years of follow-up, 15% of the participants with elevated CRP levels (>3 mg/L) were hospitalised for HF, compared with 7% of those with CRP +info)
Mechanical dyssynchrony in congestive heart failure: diagnostic and therapeutic implications.
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Cystatin C concentration as a predictor of systolic and diastolic heart failure.
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Reversal of cardiac dysfunction after long-term expression of SERCA2a by gene transfer in a pre-clinical model of heart failure.
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