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PubMed2001

Diastolic dysfunction is predictive of difficult weaning from cardiopulmonary bypass.

Diastolic function is receiving more attention since echocardiographic measurements were developed and have become widely available. The importance and significance of diastolic dysfunction (DD) observed before cardiac surgery and its relationship with adverse outcomes, such as difficult separation from cardiopulmonary bypass (CPB), have not been fully explored. In this study, we hypothesize that DD can be a predictor for the need of inotropic support to successfully separate from CPB. Ninety-two consecutive patients underwent surgery during the study period. Twenty-six patients were excluded. From the remaining 66 patients, 52 had coronary artery bypass grafting alone and 14 combined procedures, valvular surgery, and reoperations (redo). Systolic and diastolic function was evaluated by two experts blinded as to the clinical data except for the age. The evaluation of diastolic function was done according to published guidelines. The demographic, echocardiographic, and hemodynamic variables were entered in a logistic regression analysis to determine which variables were independent predictors of difficult separation from CPB and the need for postoperative vasoactive support. DD was present in 20 patients (30%). Patients with DD had lower weight (P = 0.046), less frequent coronary artery bypass grafting alone (P = 0.0004), more myocardial infarction before surgery (P = 0.02), higher regional wall motion score index (P = 0.0002), and larger left ventricle (P = 0.03). Total CPB time (P = 0.004) and ischemic time (P = 0.007) were longer in the DD group. Patients with DD required more frequent inotropic support at the end of surgery (P = 0.006) and up to 12 h after surgery (P = 0.003). Multivariate logistic regression identified female sex, DD, and total CPB time as predictive of difficult weaning and inotropic requirements up to 12 h after surgery.

Aged↗
PubMed1994

Recovery of load-induced left ventricular diastolic dysfunction by coenzyme Q10: echocardiographic study.

UNLABELLED: Load-induced cardiac dysfunction (LCD), in which a supernormal left ventricular (LV) systolic performance at rest decreases due to an afterload challenge, usually occurs among children with mitral valve prolapse (MVP). However, diastolic performance is also important because relaxation, like contraction, is based on a process that requires energy. The aim of this study was to examine LV diastolic response patterns to stress in patients with LCD before and after coenzyme Q10 (CoQ) therapy and in controls. The D-E slope, E-F slope and maximal diastolic endocardial velocity were used as echographic diastolic indices. Thirty subjects, aged 9-16 years, were divided into four groups: group 1, 10 normals; group 2, 10 patients with LCD; group 3, the same 10 as in group 2, who recovered with CoQ, 3.0-3.4 mg/kg/day for 7 days; group 4, 10 asymptomatic children with MVP. The heart rate, both at rest and during handgrip (HG), showed little intergroup difference. Only in group 2, were the ejection fraction and all the diastolic indices greater than in the other groups, but these became subnormal with HG. In the other groups, these indices increased with HG to a similar extent, although resting values were smaller than in group 2. IN CONCLUSION: (1) in normal hearts and in hearts with LCD, diastolic performance mimicked systolic performance both in resting and loading conditions; (2) CoQ improved not only the load-induced systolic but also the diastolic dysfunctions in a similar time-course, and (3) mechanical stiffness of the cardiac tissue may not be a cause of load-induced diastolic dysfunction, because the dysfunction was quickly resolved with CoQ therapy. CoQ may be a key substance which affects a common bioenergetic process in contraction and relaxation, to keep these functions normal.

Adolescent↗
PubMed1998

Pharmacological strategies for improving diastolic dysfunction in the setting of chronic pulmonary hypertension.

BACKGROUND: Right ventricular (RV) hypertrophy is an adaptive process that occurs in the setting of chronic pulmonary hypertension (CPH) and can lead to alterations in normal RV diastolic properties. This study was designed to investigate the effects of NO and milrinone on RV diastolic dysfunction in the setting of CPH and RV hypertrophy by use of a canine model of monocrotaline pyrrole (MCTP)-induced CPH. METHODS AND RESULTS: Sixteen mongrel dogs (22 to 24 kg) were used. Animals underwent percutaneous pulmonary artery (PA) catheterization to measure pulmonary hemodynamics before and 8 weeks after injection of 3 mg/kg MCTP (n=8) or placebo (control, n=8). Eight weeks after injection, all hearts were instrumented with a PA flow probe, sonomicrometric dimension transducers, and micromanometers. Data were collected at baseline and after both NO and milrinone administration. Diastolic properties were quantified by use of the end-diastolic pressure-volume relationship and the time constant of ventricular isovolumic relaxation. Eight weeks after injection, significant increases in the PA pressure and pulmonary vascular resistance were observed in MCTP dogs. Significant worsening of RV diastolic function occurred in association with significant increases in the ratio of RV dry weight to LV+septal dry weight. NO and milrinone administration both led to significant improvements in RV diastolic properties. CONCLUSIONS: In the setting of MCTP-induced CPH, significant worsening of RV diastolic function was observed in association with significant increases in the ratio of RV dry weight to LV+septal dry weight, suggesting that these changes are partially due to RV hypertrophy. The significant improvement in RV diastolic properties after both NO and milrinone administration suggests that these agents may be effective forms of pharmacological therapy for improving RV diastolic dysfunction in the setting of CPH.

Administration, Inhalation↗
PubMed1988

Enhanced sensitivity to hypoxia-induced diastolic dysfunction in pressure-overload left ventricular hypertrophy in the rat: role of high-energy phosphate depletion.

Isolated buffer-perfused rat hearts with pressure-overload hypertrophy develop a greater decrease in left ventricular (LV) diastolic distensibility and a greater impairment in extent of LV relaxation in response to hypoxia than do normal hearts. Using 31P-NMR spectroscopy, we tested the hypothesis that the enhanced susceptibility of hypertrophied hearts to develop hypoxia-induced diastolic dysfunction is due to an accelerated rate of ATP and/or creatine phosphate depletion. Twelve minutes of hypoxia were imposed on isolated isovolumic (balloon-in-left-ventricle) buffer-perfused hearts from 14 rats with pressure-overload hypertrophy (LVH; LV/body wt ratio = 3.43 +/- 17) secondary to hypertension induced by uninephrectomy plus deoxycorticosterone and salt treatment and from 17 age-matched controls (LV/body wt ratio = 2.22 +/- 0.12, p less than 0.001). Coronary artery flow per gram left ventricle was matched in the LVH and control groups during baseline oxygenated conditions and held constant thereafter. Balloon volume was held constant throughout the experiment so that an increase in LV end-diastolic pressure during hypoxia represented a decrease in LV diastolic distensibility. LV systolic pressure was 165 +/- 9 mm Hg in the LVH group compared with 120 +/- 5 mm Hg in the controls during baseline aerobic perfusion (p less than 0.001). LV end-diastolic pressure rose significantly more in response to 12 minutes of hypoxia in the LVH group (12 +/- 1 to 44 +/- 10 mm Hg) than in the controls (12 +/- 1 to 20 +/- 3 mm Hg, p = 0.04). During baseline aerobic conditions, ATP content was the same in the LVH (17.1 +/- 0.5 mumol/g dry LV wt, n = 4) and control (18.8 +/- 0.6 mumol/g dry LV wt, n = 4, p = NS) groups. During hypoxia, ATP declined at the same rate in the LVH and control groups (3.2 +/- 0.5 versus 3.0 +/- 0.5%/min, p = NS) despite the greater rise in end-diastolic pressure in the LVH group. Creatine phosphate content during baseline aerobic perfusion was 14% lower in the LVH group compared with controls, but the rate of creatine phosphate depletion during 12 minutes of hypoxia was the same. During hypoxia, intracellular pH declined modestly and to the same degree in both groups. Thus, the greater susceptibility to hypoxia-induced diastolic dysfunction observed in isolated buffer-perfused hypertrophied rat hearts cannot be explained by an initially lower total ATP content or by an accelerated rate of decline of ATP or creatine phosphate.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1997

[Diastolic dysfunction of the left ventricle: from physiopathology to treatment].

Our understanding of cardiac failure has greatly changed over the last 15 years. Left ventricular diastolic dysfunction, which is now recognised as one of the primary causes of certain types of cardiac failure (1). Abnormal left ventricular diastolic function is the common determinant and indeed the earliest sign of all chronic left ventricular failures whether systolic left ventricular dysfunction is associated with it or not (2). In this paper, we review the basis of diastolic dysfunction and its impact on diagnosis and treatment of cardiac failure.

Aged↗
PubMed1998

[Value of echocardiography and heart Doppler in the diagnosis and therapeutic orientation of congestive heart failure--the importance of diastolic dysfunction].

Echocardiography and cardiac-Doppler are very useful techniques to achieve etiologic diagnosis and evaluate therapeutic strategies for heart failure, and left ventricular hypertrophy is known as a serious risk factor for cardiovascular disease morbidity and mortality. Echocardiography establishes, in an easy and noninvasive way, the etiologic diagnosis of heart failure and is a very sensitive technique for the diagnosis and follow-up of patients with left ventricular hypertrophy. On the other hand, diastolic dysfunction is an early manifestation of several conditions associated with heart failure emerging from the diastolic mechanism. The author emphasizes the role of cardiac Doppler in the early diagnosis of diastolic dysfunction and how findings provided by this procedure can lead to more adequate therapeutic measures and assess accurate prognostic information.

Diastole↗
PubMed2000

Diastolic dysfunction in the elderly. Genesis and diagnostic and therapeutic implications.

Diastolic left ventricular function is altered substantially with advancing age in healthy persons, and diastolic dysfunction impacts most cardiovascular disorders in the elderly. Older, healthy persons have a delayed relaxation Doppler filling pattern and their early deceleration time is similar to, or modestly lengthened, compared with younger, healthy persons. Two abnormal Doppler filling patterns, the pseudo-normal and the restricted, are discerned more easily, and are more specific in the elderly than the young, because they are the opposite (reverse) of the normal elderly pattern. Most heart failure in the elderly occurs in the presence of preserved systolic function (presumed diastolic heart failure). Elderly patients with diastolic heart failure tend to be women with hypertrophied, hyperdynamic left ventricles, and chronic hypertension. Prognosis may be somewhat better than in systolic heart failure, but the difference diminishes when adjusted for gender and in the very elderly. The pathophysiology of this disorder is not well characterized, diagnostic criteria have not been standardized, and there are no large, multicenter, randomized trials to guide therapy. Further research in this area should be a high priority.

Aged↗
PubMed2001

Diastolic dysfunction and increased serum homocysteine concentrations may contribute to increased cardiovascular risk in patients with polycystic ovary syndrome.

OBJECTIVE: To assess cardiac flow parameters in patients with polycystic ovary syndrome (PCOS). DESIGN: A prospective case-control study. SETTING: University-based hospital. PATIENT(S): Thirty consecutive patients with PCOS were enrolled. Thirty women with regular menstrual cycles served as the controls. INTERVENTION(S): Systolic and diastolic function parameters were assessed by standard two-dimensional and M-mode echocardiography. Insulin sensitivity was evaluated by a standard 75-g oral glucose tolerance test and area-under-curve insulin analysis. Serum hormones, lipid profile, homocysteine, vitamin B(12), folate, fibrinogen, uric acid, and plasminogen activator inhibitor-I concentrations were measured. MAIN OUTCOME MEASURE(S): Systolic and diastolic function parameters, insulin sensitivity and serum homocysteine levels. RESULT(S): The mean serum homocysteine and uric acid concentrations were significantly higher in the PCOS group. Patients with PCOS had significant hyperinsulinemia. All systolic function parameters were comparable between the two groups. However, patients with PCOS had significantly lower peak mitral flow velocity in early diastole and significantly lower ratio between the early and late peak mitral flow velocities and also had significantly longer isovolumic relaxation time, reflecting a trend for nonrestrictive-type diastolic dysfunction. The area-under-curve insulin correlated positively with peak mitral flow velocity in late diastole (r = 0.375). The mean cholesterol/high-density lipoprotein ratio correlated negatively with mean mitral flow velocity in early diastole (E) peak (r = -0.474). The mean fasting insulin level correlated negatively with mean E/A ratio (r = -0.387). CONCLUSION(S): Diastolic dysfunction and increased serum homocysteine concentrations may contribute to increased cardiovascular disease risk in patients with PCOS.

Adult↗
PubMed1997

Severe diastolic dysfunction with preserved energy conversion efficiency after countershock.

The left ventricular (LV) mechanical performance and the LV myocardial oxygen consumption (VO2)-to-pressure-volume area (PVA; LV total mechanical energy index) relationship were measured in isovolumic contraction of isolated blood-perfused dog hearts before and after direct current (DC) countershocks. At a constant LV volume, DC shocks increased LV end-diastolic pressure progressively and strikingly with the progression of myocardial edema and a marked prolongation of the time constant of LV pressure decay. In contrast, DC shocks changed neither the slope of the LV end-systolic pressure-volume relationship nor the contractile efficiency (the slope of the Vo2-PVA relationship). The oxygen cost of contractility (the slope of the relationship between PVA-independent VO2 and LV contractility) increased 27% after DC shocks. However, the magnitude of this change was considerably smaller than that previously reported in postischemic stunned myocardium (123%), suggesting that the adverse effect of DC shocks on the energy cost of excitation-contraction coupling is relatively minor. Thus, despite the severe diastolic dysfunction, DC shocks do not substantially impair either the efficiency of cross-bridge cycling or calcium cycling. Myocardial interstitial edema is more likely a potential mechanism of diastolic dysfunction after DC shocks.

Animals↗
PubMed1991

Left ventricular diastolic dysfunction in patients with congestive heart failure.

This study reviewed 372 male patients with congestive heart failure. Two hundred and eighty-three (77%) had congestive heart failure due to systolic dysfunction as demonstrated by radionuclide angiography. Eighty-seven (23%) with congestive heart failure were identified who had normal ejection fractions. All patients met the Framingham criteria for congestive heart failure. These 87 individuals had unrecognized diastolic heart failure. It is important to distinguish between systolic and diastolic heart failure because the pathophysiology, treatment, and prognosis differ significantly. The most frequent cause of diastolic heart failure in this study was hypertension. Diastolic dysfunction should be considered in patients with acute heart failure and severe uncontrolled hypertension, or in patients with ischemic heart disease who develop acute pulmonary edema. Patients who do not respond or deteriorate when treated for heart failure using conventional therapy may also have diastolic dysfunction. These patients warrant special recognition and tailored management.

Aged↗
PubMed2002

Tei-Index in coronary artery disease--validation in patients with overall cardiac and isolated diastolic dysfunction.

BACKGROUND: The index "isovolumic contraction time and isovolumic relaxation time divided by ejection time" ("Tei-Index") has been demonstrated to provide useful information about disease severity and prognosis in patients with dilated cardiomyopathy and cardiac amyloidosis. In patients with coronary artery disease (CAD), the diagnostic utility of this index is unclear. We attempted to validate the Tei-Index in CAD patients with overall cardiac or isolated diastolic dysfunction. METHODS AND RESULTS: Sixty subjects were included who underwent left heart catheterization for invasive measurement of left ventricular end-diastolic pressure (LVEDP): 20 symptomatic CAD patients with overall cardiac dysfunction (defined by a LV ejection fraction (EF) < 45% (mean 27 +/- 8%) and a LVEDP > or = 16 mmHg, (mean 22 +/- 6 mmHg), NYHA class 2.7 +/- 0.4, OCD group), 29 symptomatic CAD patients with isolated diastolic dysfunction (defined by an EF > 45% (mean 55 +/- 8%), a normal end-diastolic diameter index (mean 2.8 +/- 0.4 cm/m2) and a LVEDP > or = 16 mmHg (mean 22 +/- 6 mmHg), NYHA class 2.3 +/- 0.4, IDD group) and 11 asymptomatic control subjects (EF 65 +/- 9%, LVEDP 11 +/- 4 mmHg, CON group). After conventional 2-D- and Doppler echocardiographic examination, the Tei-Index was obtained. The Tei-Index was easily and reproducibly measured in all study subjects. In the OCD group, isovolumic contraction time was prolonged and ejection time was shortened in comparison to the CON group, resulting in a significantly increased Tei-Index (0.71 +/- 0.28 vs 0.40 +/- 0.11, p < 0.01). In the IDD group, isovolumic relaxation time was prolonged and isovolumic contraction time was shortened in comparison to controls, resulting in a largely unchanged Tei-Index (0.45 +/- 0.14, p = ns). Receiver operating characteristic curve analysis for the Tei-Index yielded an area under the curve of 0.92 +/- 0.04 for separating patients with vs without OCD. Using a Tei-Index > 0.49 as a cut-off, OCD patients were identified with a sensitivity of 96% and a specificity of 86%. CONCLUSION: The Tei-Index is a valid and readily derived indicator of global cardiac dysfunction in CAD patients with impaired systolic and diastolic LV performance. The use of this index seems to be limited in CAD patients with primary diastolic dysfunction.

Aged↗
PubMed2001

Maturation-dependent differences in regulation of sarcoplasmic reticulum Ca(2+) ATPase in sheep myocardium in response to pressure overload: a possible mechanism for maturation-dependent systolic and diastolic dysfunction.

We have previously demonstrated that pressure-overload hypertrophy in adult sheep is associated with myocardial dysfunction whereas that in young lambs is associated with normal contractility. To probe for possible mechanisms of these age-dependent differences, we assessed mRNA expression of genes encoding critical components of myocardial Ca(2+) handling in the same animal model. We studied left ventricular myocardium of young and adult sheep with short-term (48 h) and long-term (6 wk) pressure overload induced by ascending aortic constriction. Six weeks of pressure overload induced the significant left ventricular hypertrophy (36 and 39% increase in left ventricular/body weight ratio in lambs and sheep, respectively). The Ca(2+) ATPase and Na(+)/Ca(2+) exchanger mRNA decreased with pressure overload only in the adult (p < 0.05). Ca(2+) channel mRNA was slightly increased by pressure overload regardless of age (p < 0.05). Calsequestrin, sarcoplasmic reticulum Ca(2+) release channel, or myosin heavy-chain mRNA levels did not significantly differ. In adult sheep after 6 wk of pressure overload, decreases in load-adjusted midwall shortening (systolic dysfunction) and prolongation of relaxation time constant (diastolic dysfunction) correlated with decreases in Ca(2+)-ATPase mRNA. The sarcoplasmic reticulum Ca(2+)-ATPase protein level and Ca(2+) uptake activity of isolated sarcoplasmic reticulum vesicles were depressed only in the adult with pressure-overload hypertrophy but not in the young. We demonstrated age-dependent differences in mRNA expression of Ca(2+)-handling protein genes in response to pressure overload, which preceded the occurrence of hypertrophy and myocardial dysfunction. Thus, altered expression of Ca(2+)-handling protein genes may be one of the primary responses to pressure overload rather than a phenomenon secondary to myocardial hypertrophy.

Animals↗
PubMed1995

Diastolic dysfunction is a feature of the antiphospholipid syndrome.

Recurrent thrombi, thrombocytopenia, pregnancy loss, and stroke in association with medium to high concentrations of anticardiolipin antibodies are well-recognized features of antiphospholipid syndrome. Cardiac manifestations of primary antiphospholipid syndrome (PAPS) also have been documented but involve structural and valvular heart disease. Diastolic dysfunction in PAPS has not been well described. Therefore, 10 patients with PAPS (nine women and one man) of mean age 30 +/- 7 years (range 20 to 46 years) and 10 healthy age-, sex-, weight-, and height-matched control subjects were studied by echocardiography. Anticardiolipin antibody concentrations of patients with PAPS were > 80 immunoglobulin G phospholipid units as determined by enzyme-linked immunosorbent assay. Doppler-derived parameters of left ventricular filling showed a significant association between PAPS and diastolic dysfunction compared with control, as evidenced by a decrease in peak early filling velocity (52 +/- 10 cm/sec vs 67 +/- 12 cm/sec; p < 0.01), a decrease in the ratio of peak early to peak atrial filling velocities (1.03 +/- 0.40 vs 1.52 +/- 0.28; p < 0.005), a decrease in the mean deceleration rate of early filling (338 +/- 75 cm/sec2 vs 590 +/- 227 cm/sec2; p < 0.005), and an increase in the percentage of atrial contribution to filling and deceleration time. Left ventricular mass, diastolic filling time, and heart rate did not differ between groups. Left ventricular systolic function was normal and ejection fraction did not differ between patients with PAPS and control subjects (63% +/- 2% vs 65% +/- 7%; p not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Coronary flow reserve correlates left ventricular diastolic dysfunction in patients with dilated cardiomyopathy.

The relationship between altered coronary circulation and left ventricular (LV) function in dilated cardiomyopathy (DCM) remains unclear. We used the Doppler guidewire and transthoracic echo Doppler in 24 DCM patients to investigate the relationship between coronary flow reserve (CFR) and LV systolic/diastolic function, trying to predict diastolic dysfunction and evaluate DCM severity with CFR. CFR correlated better with the deceleration time (DT) of the E-wave and the ratio of E-wave peak value to that of the A-wave (E/A) than with LV ejection fraction (EF). The optimal CFR cutoff value for predicting the restrictive pattern of transmitral flow velocity (DT = 120 msec) was 2.6 (sensitivity 91%, specificity 100%). Dividing patients into two groups around the CFR = 2.6 cutoff, differences in DT and E/A between groups were more prominent than those for EF. CFR correlates better with LV diastolic than systolic function and may be useful for predicting diastolic dysfunction in DCM patients.

Adult↗
PubMed1997

Postresuscitation left ventricular systolic and diastolic dysfunction. Treatment with dobutamine.

BACKGROUND: Global left ventricular dysfunction after successful resuscitation is well documented and appears to be a major contributing factor in limiting long-term survival after initial recovery from out-of-hospital sudden cardiac death. Treatment of such postresuscitation myocardial dysfunction has not been examined previously. METHODS AND RESULTS: Systolic and diastolic parameters of left ventricular function were measured in 27 swine before and after successful resuscitation from prolonged ventricular fibrillation cardiac arrest. Dobutamine infusions (10 micrograms.kg-1.min-1 in 14 animals or 5 micrograms.kg-1.min-1 in 5 animals) begun 15 minutes after resuscitation were compared with controls receiving no treatment (8 animals). The marked deterioration in systolic and diastolic left ventricular function seen in the control group after resuscitation was ameliorated in the dobutamine-treated animals. Left ventricular ejection fraction fell from a prearrest 58 +/- 3% to 25 +/- 3% at 5 hours after resuscitation in the control group but remained unchanged in the dobutamine (10 micrograms.kg-1.min-1) group (52 +/- 1% prearrest and 55 +/- 3% at 5 hours after resuscitation). Measurement of the constant of isovolumic relaxation of the left ventricle (tau) demonstrated a similar benefit of the dobutamine infusion for overcoming postresuscitation diastolic dysfunction. The tau rose in the controls from 28 +/- 1 milliseconds (ms) prearrest to 41 +/- 3 ms at 5 hours after resuscitation whereas it remained constant in the dobutamine-treated animals (31 +/- 1 ms prearrest and 31 +/- 5 ms at 5 hours after resuscitation). CONCLUSIONS: Dobutamine begun within 15 minutes of successful resuscitation can successfully overcome the global systolic and diastolic left ventricular dysfunction resulting from prolonged cardiac arrest and cardiopulmonary resuscitation.

Animals↗
PubMed1993

Effects of brief repetitive ischemia on contractility, relaxation, and coronary flow. Exaggerated postischemic diastolic dysfunction in pressure-overload hypertrophy.

The recovery of systolic and diastolic function during unstable angina may be modified by the repetition of brief episodes of ischemia and by the presence of left ventricular hypertrophy (LVH). We studied the effects of six consecutive 5-minute cycles of no-flow ischemia and reperfusion followed by 25 minutes of recovery in isovolumic red blood cell-perfused hearts from aortic-banded rats with chronic LVH (n = 8) and sham-operated control rats (n = 8). At baseline (left ventricular end-diastolic pressure [LVEDP], 10 mm Hg), left ventricular developed pressure (123 +/- 5 versus 114 +/- 5 mm Hg/g) and coronary flow [2.5 +/- 0.3 versus 2.2 +/- 0.2 (mL/min)/g] were similar in LVH versus control rats. Repetitive ischemia was associated with progressive depression of postischemic recovery of left ventricular systolic function, and the recovery of left ventricular developed pressure after the final 25-minute reperfusion period was similar in LVH versus control rats (61 +/- 6% versus 72 +/- 4% of baseline, P = NS). Although there was no increase in isovolumic LVEDP during the initial cycle of transient ischemia, both groups showed a rapid and similar rise in LVEDP during subsequent ischemic cycles (delta 82 +/- 8 versus delta 89 +/- 7 mm Hg/g in response to the final ischemia cycle for LVH versus control rats, respectively; P = NS). The control hearts showed complete restoration of LVEDP to baseline during final reperfusion, whereas the LVH hearts showed prolonged and severe postischemic diastolic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

[Observation of enalapril on treating the patients with left ventricular diastolic dysfunction].

The effects of enalapril on 50 patients with left ventricular diastolic dysfunction (LVDD), confirmed by clinical features and radionuclid ventriculography, were assessed in a randomized, double-blind, and controlled method for eight weeks. The results showed that left atrial diameters (LAD), interventricular septum thicknesses (IVST) and left ventricular mass indexes (LV-MI) except left ventricular diameters (LVD) were decreased in the enalapril treatment group. The left ventricular diastolic function parameters such as the early peak filling velocity (EPAV), the atrial peak filling velocity (APAV), the deceleration of early peak filling velocity (DC) and the isovolumic relaxation time (IRT) were improved, the NYHA class and the exercise tolerance were increased, the left ventricular ejection fraction (LVEF), and the cardiac index (CI) were not altered in the enalapril treatment group. The patients with LVDD were well tolerated with enalapril. The parameters mentioned above were not altered in control group. It is suggested that enalapril is an effective drug in the treatment of LVDD.

Adult↗
PubMed1992

Diastolic dysfunction in pressure-overload hypertrophy and its modification by angiotensin II: current concepts.

Cardiac hypertrophy is an adaptive response to an increased load imposed on the myocyte which allows the heart to perform increased work while maintaining normal myocardial fiber stress and shortening in systole. A deleterious consequence of pressure-overload hypertrophy is the prolongation of Ca(2+)-sensitive force inactivation (impaired myocardial relaxation) which is related to intrinsic alterations in cytosolic Ca2+ transport and reuptake in diastole. Additional factors appear to adversely modify myocardial relaxation in the hypertrophied heart, including the imposition of ischemia. There is also evidence that the expression and activity of the cardiac tissue renin angiotensin system (RAS) may be modified in the hypertrophied heart and contribute to diastolic dysfunction. Recent studies have demonstrated the presence of increased cardiac angiotensin converting enzyme (ACE) mRNA expression and activity in animal models of hypertrophy, including the aortic-banded rat with compensatory pressure-overload hypertrophy and rats with post-infarction remodeling. In the beating, isovolumic aortic-banded rat heart, the increased intracardiac activation of angiotensin I to II has been shown to be associated with a dose-dependent depression of diastolic relaxation. Preliminary studies suggest that the depression of diastolic function by angiotensin II in the hypertrophied heart can be prevented by the specific inhibition of cardiac ACE. In addition, the well-recognized susceptibility of the hypertrophied heart to severe ischemic diastolic dysfunction also appears to be favorably modified by the inhibition of cardiac ACE activity. The mechanisms responsible for the adverse effects of angiotensin II on diastolic relaxation in the hypertrophied heart are likely to be complex.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗