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PubMed1990

Influence of glucose and insulin on the exaggerated diastolic and systolic dysfunction of hypertrophied rat hearts during hypoxia.

Myocardial hypertrophy can result in increased sensitivity toward the development of mechanical dysfunction during hypoxia. Alterations in glycolytic metabolism may contribute to this. We studied the response to 15 minutes of hypoxia in hypertrophied (deoxycorticosterone-salt hypertension model) and nonhypertrophied rat hearts and examined the influence of a high glucose (27.5 mM) and insulin (100 mU/ml) concentration. In response to hypoxia in the presence of a normal glucose concentration (5.5 mM), left ventricular end-diastolic pressure was higher in hypertrophied than in nonhypertrophied hearts (65 +/- 6 vs. 44 +/- 4 mm Hg; p less than 0.05). Perfusion with high glucose and insulin blunted the rise in left ventricular end-diastolic pressure in both hypertrophied and nonhypertrophied hearts and abolished the difference in diastolic dysfunction between groups during hypoxia (26 +/- 2 vs. 32 +/- 4 mm Hg, respectively; p = NS). At end hypoxia in the presence of a normal glucose concentration, developed pressure was more depressed in hypertrophied than in nonhypertrophied hearts (11 +/- 1 vs. 18 +/- 1% of baseline, respectively; p less than 0.05). Perfusion with high glucose and insulin resulted in improved function in both groups during hypoxia such that a greater impairment of developed pressure was no longer present in the hypertrophied versus nonhypertrophied hearts (21 +/- 1 vs. 24 +/- 2% of baseline, respectively; p = NS). At the end of hypoxic perfusion in the presence of a normal glucose concentration, hypertrophied hearts were producing 38% less lactate than nonhypertrophied hearts. Perfusion with high glucose and insulin increased lactate production in both groups and equalized lactate production between groups. Thus, the greater deterioration in hemodynamic function in hypertrophied hearts compared with nonhypertrophied hearts during hypoxia is associated with lower lactate production. Both the exaggerated hemodynamic dysfunction and deficient lactate production can be ameliorated by perfusion with a high glucose concentration and insulin.

Animals↗
PubMed1990

Thallium 201 kinetics in stunned myocardium characterized by severe postischemic systolic dysfunction.

The hypothesis tested in this study was that despite the presence of severe postischemic myocardial dysfunction ("stunning"), the extraction and subsequent intracellular washout of thallium 201 should be preserved as long as irreversible sarcolemmal membrane injury was avoided. To produce myocardial stunning, 19 open-chested dogs with a critical left anterior descending coronary artery (LAD) stenosis underwent 10 5-minute periods of total LAD occlusion, each interspersed by 10 minutes of reperfusion by reflow through the critical stenosis. In another 12 control dogs observed for the same time period, no LAD occlusions were performed after placement of the critical stenosis. Hemodynamics, regional myocardial thickening by quantitative two-dimensional echocardiography, and microsphere-determined regional blood flows were serially measured. In 18 stunned dogs, systolic thickening in the LAD zone was markedly reduced to 0.4 +/- 2.4% at 40 minutes after the 10th reperfusion period compared with 32.5 +/- 2.2% thickening (p less than 0.001) in 12 control dogs at a matched time. The 201Tl first-pass extraction fraction determined by a double-isotope method using intracoronary 201Tl administration was comparable after the 10th reflow in a subgroup of 13 stunned (0.78) and six control (0.79) dogs. The T1/2 for the intracellular washout rate was also not significantly different in another group of six stunned (60 +/- 13 minutes) and six control (53 +/- 14 minutes) dogs, nor was the percentage of the 201Tl dose initially distributed in the interstitial compartment (11 +/- 3% vs. 7 +/- 2%). Systemic hemodynamics and regional flows were comparable in the two groups at 40 minutes after the 10th reflow. No dog had evidence of myocardial necrosis by triphenyl tetrazolium chloride staining. Thus, normal myocardial 201Tl extraction and washout kinetics are observed in a canine model of severe postischemic dysfunction (stunning) produced by repetitive brief LAD occlusions. These findings might have important clinical implications concerning the application of rest 201Tl scintigraphy for evaluation of perfusion and viability in patients with coronary artery disease and regional myocardial asynergy that is ultimately reversible.

Animals↗
PubMed1996

Hemodynamic and cardiac effects of the selective T-type and L-type calcium channel blocking agent mibefradil in patients with varying degrees of left ventricular systolic dysfunction.

OBJECTIVES: This study sought to assess the hemodynamic and cardiac effects of two dose levels of mibefradil in patients with varying degrees of ischemic left ventricular dysfunction. BACKGROUND: Mibefradil is a new, selective T-type and L-type calcium channel blocking agent. Because L-type channel blockade may depress myocardial performance, an invasive hemodynamic study was performed to assess the safety of this agent. METHODS: We performed an open label study, examining the effects of two intravenous doses of mibefradil, selected to produce plasma levels comparable to those measured after oral administration of 50 mg (dose 1: 400 ng/ml) or 100 mg (dose 2: 800 ng/ml) of the drug. Variables studied included the indexes of left ventricular function and neurohormone levels. Patients were stratified according to ejection fraction (EF) (> or = 40%, n = 26; < 40%, n = 24) and the presence (n = 15) or absence (n = 35) of heart failure. RESULTS: In patients with preserved systolic function, dose 1 had no clinically significant hemodynamic effects, but dose 2 decreased mean aortic pressure and systemic vascular resistance (-8.5 mm Hg, -12%, both p < 0.01) and also reduced end-systolic stress and volume, thus improving EF (52% to 58%, p < 0.01). Heart rate tended to decrease. In patients with depressed EF, heart rate decreased significantly with both doses. The effects of dose 1 mimicked those observed after dose 2 in patients with preserved EF. Dose 2 (plasma levels 1,052 +/- 284 ng/ml) still decreased left ventricular systolic wall stress and improved EF (24.0% to 28.5%, p < 0.05) but also significantly depressed the maximal first derivative of left ventricular pressure. Examination of individual pressure-volume loops in two patients with heart failure showed a clear rightward shift of the loop despite a decrease in systolic pressure, suggesting negative inotropy. Neurohormone levels were unchanged at both dose levels and in all subgroups. CONCLUSIONS: Intravenous mibefradil was well tolerated and produced an overall favorable cardiovascular response. However, high plasma concentrations might produce myocardial depression in patients with heart failure, and caution should be exerted in this setting.

Adult↗
PubMed2003

Left ventricular remodelling and haemodynamic effects of multisite biventricular pacing in patients with left ventricular systolic dysfunction and activation disturbances in sinus rhythm: sub-study of the MUSTIC (Multisite Stimulationin Cardiomyopathies) trial.

AIMS: To use echocardiography to determine early and late haemodynamic effects of atrio-biventricular (A-BiV) pacing on left ventricular (LV) function and their interrelations with exercise tolerance. METHODS: Thirty-four patients with ejection fraction <35% (18 idiopathic dilated cardiomyopathy (DCM) and 16 ischaemic cardiomyopathy, in sinus rhythm and with intra-ventricular conduction delay (IVCD)) were implanted with transvenous A-BiV pacemakers. Echocardiographic measurements were compared before implantation, after 3 months A-BiV pacing, and 3 months inactive pacing (ventricular inhibited pacing at 40 beats x min(-1)as part of a crossover design, and at 9- and 12-month longitudinal follow-up. RESULTS: Total isovolumic time (IVT) halved after 3 months A-BiV pacing (from 20.1+/-4.4 to 10.7+/-4.9s min(-1), P<0.001) and did not change thereafter. LV cavity size fell after 3 months (end-diastolic dimension (EDD) 7.3+/-0.8 to 6.8+/-0.8 cm, P<0.001, and end-systolic dimension (ESD) 6.2+/-0.8 to 5.9+/-0.8 cm, P<0.05), with a further fall in EDD and ESD (by 8.4+/-7.8 and 8.8+/-7.8mm, respectively, both P<0.001) after 12 months. Although not a primary end-point of the study, the 12-month reduction in LVEDD and LVESD was greater in idiopathic DCM (by 8.9 and 9.8mm, P<0.01, respectively) compared with ischaemic cardiomyopathy. The 6-min walk rose by 15% (P<0.01) and peak VO(2)by 10% (P<0.05) after 3 months, with no further increase by 12 months, and no difference between idiopathic DCM and ischaemic cardiomyopathy. The increase in peak VO(2)at 12 months correlated with the fall in ESD (r=0.47, P=0.03). CONCLUSIONS: A-BiV pacing shortens total IVT, reduces LV cavity size, and increases exercise tolerance in patients with DCM and IVCD. Ischaemic cardiomyopathy does not affect the exercise response, although it does reduce the extent of reverse remodelling.

Aged↗
PubMed2000

QT interval lengthening in cardiac disease relates more to left ventricular systolic dysfunction than to autonomic function.

BACKGROUND: There are multiple influences on the QTc interval, including the autonomic nervous system. Which influence is the principal determinant of the variation in QTc interval between different cardiac diseases is not yet clear, though some studies have suggested that the QTc interval primarily reflects sympatho-vagal balance. This study investigated this claim further. AIM: To determine if autonomic tone was the prime determinant of variation in the QTc interval between subjects with different cardiac diseases. METHODS: Subjects with different cardiac diseases were studied, QTc interval determined and correlated with three different measures of the autonomic nervous system, that of baroreflex sensitivity, catecholamine levels (epinephrine and norepinephrine) and sympatho-vagal balance as determined by power spectrum analysis. RESULTS: 47 subjects were studied, comprising 17 subjects with heart failure, 14 subjects with left ventricular hypertrophy and 16 control subjects. For the group as a whole there was no relationship between QTc interval and any measure of the autonomic nervous system function, but there was a reasonable relationship between fractional shortening and QTc interval (r=0.47, P<0.003). For subjects with an echocardiographic fractional shortenings less than 0.35 (which correlates with an ejection fraction of <50%), a strong relationship between fractional shortening and QTc interval remained (r=0.57, P<0.002), but in addition a relationship between QTc interval and catecholamine levels developed (for epinephrine: r=0.67, P<0.002; and for norepinephrine: r=0.62, P<0.005). Multiple regression analysis showed that fractional shortening and epinephrine levels were independently related to QTc interval. CONCLUSION: In subjects with a variety of cardiac diseases, the prime determinant of QTc interval is left ventricular systolic performance rather than the autonomic nervous system, though in subjects with low normal and less fractional shortenings catecholamine levels are independently related to QTc interval.

Autonomic Nervous System↗
PubMed2000

Drug therapy of heart failure caused by systolic dysfunction in the elderly.

The presence of multiple medical illnesses often distinguishes elderly patients with heart failure and can make pharmacologic management of symptomatic heart failure challenging in this population. Physiologic changes that occur with normal aging may complicate clinical assessment. Limited data from large clinical trials of heart failure therapy are applicable to aged patients. Available data suggest that elderly patients should be treated with the same regimen as younger patients but that more careful attention should be paid to dosing, especially when initiating a new drug. History and physical examination techniques can be used to uncover evidence of congestion and inadequate perfusion and are critical adjuncts when making therapeutic decisions. The objectives of therapy for elderly patients with heart failure must be individualized within the larger context of patients' goals and stage of life.

Adrenergic Antagonists↗
PubMed1993

Is left ventricular systolic dysfunction in hypertensive patients with heart failure normalized by long-term antihypertensive therapy?

The critical left ventricular (LV) mass when hypertensive heart failure appears, and whether LV dysfunction in hypertensives with heart failure is normalized by long-term antihypertensive therapy were investigated. LV dimension, LV mass, LV mass index, LV ejection time (LVET) and pre-ejection period (PEP) were measured in 27 normal subjects and 56 essential hypertensives, the latter divided into three groups: group I, without LV hypertrophy; group II, with LV hypertrophy; and group III, with hypertensive heart failure. LV mass and LV mass index were 135.0 +/- 23.8 g and 85.8 +/- 11.7 g/m2, respectively, in normal controls, 133.0 +/- 30.8 g and 82.0 +/- 18.4 g/m2 in group I, 222.3 +/- 38.0 g and 136.1 +/- 19.9 g/m2 in group II, and 422.0 +/- 30.3 g and 235.7 +/- 19.6 g/m2 in group III of essential hypertensives. The upper limits of LV mass and LV mass index in group II (mean + 2SD) were about 300 g and 180 g/m2, respectively. Significant shortening of LVET was observed only in group III, but PEP was prolonged with an increase in LV mass. LV diastolic dimension and PEP were not normalized by long-term antihypertensive therapy (mean: 16 months). These results indicate that the critical LV mass marking the transition from non-failing hypertrophied left ventricle to failing ventricle associated with essential hypertension is about 300 g, or LV mass index of 180 g/m2, and that LV dilatation and depressed myocardial contractility in essential hypertensives with a past history of congestive heart failure were not normalized by chronic antihypertensive therapy.

Adult↗
PubMedDate not supplied

Management of heart failure. IV. Anticoagulation for patients with heart failure due to left ventricular systolic dysfunction.

OBJECTIVE: This article reviews the incidence of arterial thromboembolism in patients with heart failure who are not receiving anticoagulants. We also examine whether more severe ventricular dysfunction increases this incidence and the efficacy and risks of anticoagulation for patients in sinus rhythm. DATA SOURCES: English-language studies referenced in MEDLINE or EMBASE (January 1966 to September 1993) were reviewed. We used the search terms heart failure, congestive; congestive heart failure; heart failure; cardiac failure; and dilated cardiomyopathy in conjunction with the terms anticoagulation, cerebrovascular disorders, stroke, and thromboembolism. STUDY SELECTION: All studies with separate data for patients with chronic heart failure not receiving anticoagulants were included. Articles addressing valvular heart disease or heart failure secondary to acute myocardial infarction or Chagas' disease were excluded. Studies of the occurrence of left ventricular mural thrombi were also reviewed. DATA EXTRACTION AND SYNTHESIS: Inclusion and exclusion criteria, prevalence of atrial fibrillation, mean follow-up, and the occurrence of arterial thromboembolic events were extracted. If the incidence was not given, this was estimated using the proportion of patients with events divided by the mean follow-up. CONCLUSION: The incidence of arterial thromboembolism ranged from 0.9 to 5.5 events per 100 patient-years, with the largest studies reporting incidence of 2.0% and 2.4%. Findings regarding the relationship between ventricular function and thromboembolic events are contradictory. No controlled trial has assessed the efficacy or risks of anticoagulation for patients with heart failure and sinus rhythm, and reported efficacy in case series ranged from 0% to 100%. Until adequate studies are performed, anticoagulation should be discouraged for patients with heart failure who are in sinus rhythm.

Anticoagulants↗
PubMed2004

Apolipoprotein E epsilon4 allele is associated with left ventricular systolic dysfunction.

BACKGROUND: Apolipoprotein (APOE) epsilon4 allele has been associated with cardiac dysfunction in Alzheimer's disease and beta-thalassemia. We investigated the association between APOE genotypes and left ventricular dysfunction in a population of community-dwelling elderly subjects. METHODS: This study was performed in the Rotterdam Study, a population-based prospective cohort study among elderly subjects. For 2206 participants, a baseline echocardiogram and blood specimens for APOE typing were available. Cardiac dysfunction was considered present when fractional shortening was or=65 years. CONCLUSION: The APOE epsilon4 allele is an independent risk factor for cardiac dysfunction in elderly people. Besides well-known effects on atherosclerosis and cholesterol levels, there may be other mechanisms, such as apoptosis, through which this allele exerts negative effects on myocardial performance.

Age Factors↗
PubMed2003

Systolic dysfunction is a predictor of long term mortality in men but not in women with heart failure.

AIMS: To evaluate possible gender differences in clinical profile and outcome of patients hospitalised with heart failure. METHODS AND RESULTS: During 1996 a total of 1065 hospital in-patients had confirmed heart failure, with follow-up data through 2002. Women (58%) were significantly older, had higher prevalence of hypertension and diabetes, and lower prevalence of ischaemic heart disease, chronic pulmonary disease and alcoholism. The proportion of patients with normal left ventricular ejection fraction (LVEF) increased with age, but in all age groups women had normal LVEF more frequently than men. Echocardiography was performed less frequently in females: 62% vs. 71% in men, P<0.01, and this finding was consistent in all age groups. During follow-up (median 19 months) 507 patients died (216 men [48.8%] and 291 women [46.8%]). Gender was not a predictor of survival when LVEF was included in the model (RH Male Gender 0.8, 95% CI 0.6 to 1.1, P=0.2). There was a significant interaction gender-LVEF (P=0.048): survival was similar in both genders with LVEF >0.3 but women with LVEF </=0.3 had a better prognosis than their male counterparts. CONCLUSIONS: Survival is similar in women irrespective of LVEF and in men with LVEF >0.3 while men with severely depressed LVEF have a worse prognosis.

Adolescent↗