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Effects of calcium antagonists on left ventricular structure and function.

Effects of calcium antagonists on left ventricular hypertrophy: The goals of antihypertensive treatment are to lower systemic blood pressure and to reverse left ventricular hypertrophy. A number of different drugs can induce a decrease in left ventricular mass, some of which are calcium antagonists. In particular, verapamil, diltiazem and a number of dihydropyridines (nifedipine, isradipine, lacidipine) have proved effective in this respect. Left ventricular systolic function: Left ventricular systolic function is often normal at rest in patients with hypertension, but is quite commonly abnormal during exercise. Calcium antagonists therefore do not affect resting systolic function in this category of hypertensive patients. In contrast, in hypertensive patients with heart failure the administration of dihydropyridines improves systolic performance. Left ventricular diastolic function: Isovolumic relaxation and rapid filling are often impaired in patients with hypertension, with or without left ventricular hypertrophy. Verapamil is effective in abolishing this diastolic dysfunction when given intravenously; in contrast, medium-term therapy with calcium antagonists such as diltiazem or dihydropyridines does not improve left ventricular filling properties. However, when antihypertensive therapy achieves a reduction in left ventricular mass, a consistent improvement in diastolic properties occurs.

Antihypertensive Agents↗

[Heart disease in acromegaly. Study of 27 patients].

BACKGROUND: The patients with acromegaly have an increased propensity to develop cardiovascular complications. The aim of this study was to evaluate the most relevant clinic, echocardiographic and Holter recording findings in acromegaly and its correlation with the growth hormone (GH) levels and duration of the disease. PATIENTS AND METHODS: 27 patients with acromegaly were evaluated. The basal levels of GH and insulin-like growth factor 1 (IGF-1) were measured at the time of cardiological study and compared with the spontaneous GH secretion during 12-24 hours previously studied. Echocardiogram was made using complete M-mode, two dimensional and spectral Doppler ultrasound mechanical system. Additionally an standard EKG and a Holter recording were performed during 24 hours. RESULTS: There was a strong correlation between basal levels of GH and integrated concentration of GH during the study of spontaneous secretion (r = 0.92; p < 0.01). The prevalence of symptomatic cardiovascular complications in this study was 49%, including 3 patients who died for cardiovascular events. The echocardiographic study showed a high prevalence of left ventricular hypertrophy (66.7%), diastolic dysfunction (63%) and impaired systolic function (18.5%). There was no correlation between GH and IGF-1 levels and echocardiographic findings. Conversely the degree of hypertrophy was related to the duration of the disease and the presence of arterial hypertension. The diastolic function only was related with the presence of hypertension. We found supraventricular arrhythmic events and malignant premature ventricular complexes in 6 and 6 patients, respectively. The EKG showed a high fiability to detect ventricular hypertrophy but no rhythm events. CONCLUSIONS: The high prevalence of cardiovascular complications in acromegaly, most of them asymptomatic, and its clinical relevance, advise the necessity to perform systematic cardiovascular evaluation in these patients.

Acromegaly↗

Triphasic mitral inflow velocity with middiastolic filling: clinical implications and associated echocardiographic findings.

To explore underlying mechanisms and clinical implications of middiastolic filling, we measured early and late mitral inflow velocities, deceleration time of early mitral inflow velocity, and early diastolic mitral annular velocity (E') recorded by pulsed wave Doppler echocardiography in 3 cardiac cycles of 35 patients with prominent mitral inflow (middiastolic flow velocity > or = 0.2 m/s). E' was measured at the septal corner of the mitral annulus by Doppler tissue echocardiography from the apical 4-chamber view and was found to be reduced (E' < 0.1 m/s) in all patients; early mitral inflow velocity/E' ratio was > 10 in all but 1 patient. Valsalva maneuver unmasked delayed relaxation in 15 (88%) of 17 patients and abolished middiastolic filling in 10 (59%). Triphasic mitral inflow with middiastolic flow is related to elevated filling pressure, delayed myocardial relaxation, and slow heart rate, indicating advanced diastolic dysfunction.

Aged↗

Calcium channel blockers in cardiac failure.

Congestive cardiac failure is an increasingly prevalent syndrome associated with a high morbidity and mortality. The role of calcium channel blockers in the treatment of heart failure is unclear. The potential benefits of these agents derive not only from their vasodilator properties, but also from anti-ischemic effects, beneficial effects on endothelial function and the development of atherosclerosis, and favorable effects on calcium cycling at a molecular level. Pitted against this array of potential benefits are direct negative inotropic effects and the potential for neuroendocrine activation. Treatment with short-acting dihydropyridine agents has not resulted in long-term clinical benefits in patients with cardiac failure. Diltiazem may be beneficial in patients with nonischemic heart failure, and verapamil has a neutral effect in cardiac failure, although it may have a role in combination with ace inhibition. To date, amlodipine has been associated with the most promising results, with evidence of a mortality benefit in nonischemic heart failure. Mibefradil is of no benefit in the management of heart failure, although the trend toward increased mortality in the treatment arm of the Mortality Assessment in Congestive Heart Failure (MACH)-1 trial may have been due to drug interactions. The potential role of calcium blockers in diastolic dysfunction and in combination with ace-inhibition requires further study.

Angiotensin-Converting Enzyme Inhibitors↗

Evidence for reduced coronary flow reserve in patients with insulin-dependent diabetes. A possible cause for diabetic heart disease in man.

UNLABELLED: In diabetic heart disease myocardial, interstitial, coronary and neural structures are often involved. Coronary microangiopathy is supposed to contribute an essential part, which has not yet been clearly analysed. METHODS: In 9 normotensive patients with insulin-treated diabetes (DP) with clinically suspected coronary heart disease but normal epicardial coronary arteries, coronary microcirculation was studied. Coronary flow was determined as the quotient of base line and minimal coronary resistance after dipyridamole (0.5 mg/kg i.v.), using the argon-gas-chromatography method. Systolic left ventricular function was analysed by ventriculography, diastolic function by M-Mode-echocardiography and Doppler-echocardiograhy. Twelve normotensive subjects served as control group (CON). RESULTS: In diabetic patients maximal coronary flow was significantly reduced (172 +/- 5 versus 395 +/- 103 ml/min x 100 g, p < or = 0.001) and minimal coronary resistance increased (0.6 +/- 0.19 versus 0.24 +/- 0.06 mmHg x min x 100 g/ml, p < 0.001). Coronary reserve in diabetics was markedly reduced (1.84 +/- 0.39 versus 4.23 +/- 0.52, p < or = 0.001). Global systolic function was normal in all patients (EF: DP: 72 +/- 13 versus CON: 77 +/- 12%, n.s.; cardiac index: DP: 3.2 +/- 0.8 versus CON: 3.3 +/- 1.2 1/ min x m2, n.s.). Diastolic function was impaired in diabetics with an increased relaxation time index (97 +/- 23 versus 45 +/- 18 msec, p < or = 0.01) and an impaired diastolic inflow pattern, indicated by the E/A-ratio (0.75 +/- 0.14 versus 1.66 +/- 0.13, p < or = 0.05). CONCLUSIONS: The reduced coronary flow reserve in patients with insulin-treated diabetes mellitus may play a crucial role in the pathophysiology of diabetic cardiopathy, causing myocardial ischaemia due to a disturbance of coronary microcirculation leading to diastolic dysfunction and progressing assumably to systolic failure.

Cholesterol↗

Resting and dobutamine stress echocardiographic factors associated with the development of occult dilated cardiomyopathy in healthy Doberman pinscher dogs.

In 29 healthy Doberman Pinschers, echocardiographic parameters evaluating systolic and diastolic function were examined prospectively at rest and during dobutamine constant rate infusion (5 micrograms/kg/minute) to determine if any parameters were associated with the development of occult dilated cardiomyopathy (DCM). A resting echocardiogram was repeated 1 year later to determine which dogs had met our criteria for occult DCM. Six dogs developed occult DCM during the follow-up period. Univariate logistic regression analysis showed that at rest, an increased left ventricular internal dimension in systole (LVID-S) (P = .02), preejection period (PEP) (P = .03), ratio of PEP to left ventricular ejection time (P = .02), and isovolumic relaxation time (P = .02) were significantly associated with the development of occult DCM. During dobutamine stress echocardiography (DSE), high LVID-S (P = .02) and systolic wall stress index (P = .04) and reduced fractional shortening (P = .02) and ratio of peak early to late diastolic mitral filling velocity (E/A) (P = .05) were associated with the development of occult DCM. Multiple logistic regression showed that LVID-S (P = .002) and E/A (P = .002) measured during dobutamine infusion also were associated with the development of occult DCM. Reclassification based on the DSE data was not significantly different than reclassification based on the resting echocardiographic data. Resting echocardiography and DSE have the potential to be clinically applicable screening tests for very early systolic and diastolic dysfunction in Doberman Pinschers, heralding the onset of occult DCM as it is currently defined.

Animals↗

Transmural distribution of three-dimensional systolic strains in stunned myocardium.

BACKGROUND: Regional function in stunned myocardium is usually thought to be more depressed in the endocardium than the epicardium. This has been attributed to the greater loss of blood flow at the endocardium during ischemia. METHODS AND RESULTS: We measured transmural distributions of 3D systolic strains relative to local myofiber axes in open-chest anesthetized dogs before 15 minutes of left anterior descending coronary artery occlusion and during 2 hours of reperfusion. During ischemia, regional myocardial blood flow was reduced 84% at the endocardium and 32% at the epicardium (P<0.005, n=7), but changes in end-systolic fiber length from baseline were transmurally uniform. Relative to baseline, radial segments in stunned tissue were significantly thinner at the endocardium than the epicardium at end systole (24+/-5% versus 16+/-3%; P<0.05, n=8), consistent with previous reports. Unlike radial and cross-fiber segments, however, the increase of end-systolic fiber lengths in stunned myocardium had no significant transmural gradient (23+/-8% epicardium versus 21+/-4% endocardium). We also observed significant 3D diastolic dysfunction in the ischemic-reperfused region transmurally. CONCLUSIONS: Myocardial ischemia/reperfusion in the dog results in a significant transmural gradient of dysfunction between epicardial and endocardial layers in radial and cross-fiber segments, but not for fiber segments, despite a gradient in blood flow reduction during ischemia. Perhaps systolic fiber dysfunction rather than the degree of perfusion deficit during the preceding ischemic period may be the main determinant of myocardial dysfunction during reperfusion.

Animals↗

Myocardial collagen remodeling and left ventricular diastolic function.

1. The myocardial collagen matrix is an active participant in determining ventricular architecture and diastolic function, and myocardial structural integrity and mechanical properties. It consists of a network of fibrillar collagen which is intimately related with the myocyte, myofibril and muscle fiber as well as the coronary vasculature. Consisting primarily of collagen types I and III, this material exhibits a high tensile strength which, even though normally present in relatively small amounts, plays an important role in the behavior of the ventricle during diastole. 2. Removal of less than half of the normal amount of collagen results in a dilated ventricle with increased compliance. Collagen degradation of this magnitude and similar myocardial and ventricle with increased compliance. Collagen degradation of this magnitude and similar myocardial and ventricular histologic and functional alterations are evident during ischemia and in dilated cardiomyopathy. Thus, it would appear that a chronic change in the shape and size of the heart must be preceded by alterations in the interstitial collagen matrix. 3. With elevations in the circulating levels of angiotensin and/or mineralocorticoids, the hypertrophic response of the myocardium to the accompanying hypertension includes a progressive remodeling of the collagen component. Typically there is an increase in collagen concentration, thickening of existing fibrillar collagen and the addition of new collagen at all levels of the matrix. The consequences of this remodeling are an adverse alteration of the passive mechanical properties of the myocardium and LV diastolic dysfunction. This pathophysiologic aspect of the hypertrophic process is independent of the concomitant remodeling of the myocyte.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Treatment of post resuscitation myocardial dysfunction: aortic counterpulsation versus dobutamine.

BACKGROUND: Post resuscitation myocardial stunning is well described and recognized as a significant contributor to poor long-term outcome following cardiac arrest. Optimal strategies for treatment have not been determined. METHODS: Ten domestic swine (49+/-3 kg) underwent 15 min of untreated ventricular fibrillation before being successfully resuscitated. Left ventricular systolic and diastolic function was measured at pre-arrest baseline, at 30 min and at 6 h post resuscitation. Five animals were treated immediately after resuscitation with intra-aortic balloon counterpulsation (IABP) and five were given dobutamine (5 mcg/kg per min). RESULTS: No baseline differences were found. At 30 min post resuscitation pulmonary capillary wedge pressure and LVEDP were significantly higher (16+/-3 vs. 7+/-1 and 20+/-2 vs. 11+/-1 mmHg) while LV isovolumic relaxation ('Tau') was significantly longer (34+/-2 vs. 20+/-2 ms) in the IABP treated versus the dobutamine treated animals. Likewise, at 6 h post resuscitation LV ejection fraction was significantly less (21+/-6 vs. 39+/-4%), and LVEDP significantly higher (18 vs. 10 mmHg) in the IABP group. Heart rate was not different between the groups at any time post resuscitation. CONCLUSION: Dobutamine was superior to IABP for treatment of post resuscitation left ventricular systolic and diastolic dysfunction. The hypothesized advantage of IABP for treatment of post resuscitation myocardial stunning without excessively raising the heart rate like dobutamine was not realized.

Animals↗

Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

OBJECTIVE: Rapid ventricular pacing produces a reliable model of heart failure. Cessation after 4 weeks of rapid ventricular pacing results in rapid normalization of left ventricular function, but the left ventricle remains persistently dilated. We present novel data that show that prolonged rapid ventricular pacing (10 weeks) creates a model of chronic left ventricular dysfunction. METHODS: In 9 dogs undergoing 10 weeks of rapid ventricular pacing, left ventricular function and volumes were serially assessed by using 2-dimensional echocardiography and pressure-volume analysis for 12 weeks after cessation of pacing. RESULTS: Increased end-diastolic volume and decreased systolic and diastolic function were seen at the end of pacing. By 2 weeks of recovery from rapid ventricular pacing, end-diastolic volume and ejection fraction were partially recovered but did not improve further thereafter. Load-independent and load-sensitive indices of function obtained by pressure-volume analysis at 8 and 12 weeks of recovery confirmed a persistence of both systolic and diastolic dysfunction. In addition, left ventricular mass increased with pacing and remained elevated at 8 and 12 weeks of recovery. Four of these dogs studied at 6 months of recovery showed similar left ventricular abnormalities. CONCLUSION: Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

Animals↗

Echocardiographic evaluation in patients with autosomal dominant polycystic kidney disease and end-stage renal disease.

Cardiovascular abnormalities have been considered important extrarenal manifestations of autosomal dominant polycystic kidney disease (ADPKD). However, little is known about their prevalence in patients with ADPKD undergoing hemodialysis (HD). To investigate whether cardiac abnormalities are more prevalent in these patients, clinical and echocardiographic manifestations of cardiovascular disease were evaluated in a group of 32 patients with ADPKD and a matched control group of 32 patients without diabetes treated by chronic HD for more than 6 months. Predialysis systolic and diastolic blood pressure (BP), prevalence of hypertension, and number of patients requiring antihypertensive medications were lower in the ADPKD group than controls. There was no difference in the prevalence of cardiac events, including cardiac failure, ischemic heart disease, and arrhythmia. Systolic dysfunction, diastolic patterns, and left ventricular hypertrophy were similar in the two groups. In patients with ADPKD, simple regression analysis showed left ventricular mass (LVM) index was correlated with hemoglobin level and predialytic systolic and diastolic BPs. In multiple regression analysis, predialysis systolic BP was the only independent variable linked to LVM index. The prevalence of aortic, mitral, and tricuspid valve disease did not differ between groups. In conclusion, the occurrence of cardiovascular complications in patients with ADPKD is similar to that of HD patients with other primary renal diseases, although hypertension is less prevalent.

Aged↗

Diaspirin cross-linked hemoglobin fails to improve left ventricular diastolic function after fluid resuscitation from hemorrhagic shock.

In severe hemorrhagic shock, left ventricular (LV) diastolic dysfunction is an early sign of cardiac failure due to compromised myocardial oxygenation. Immediate fluid replacement or, in particular, administration of a hemoglobin-based oxygen carrier (diaspirin cross-linked hemoglobin; DCLHb) improves myocardial oxygenation; therefore, positive effects on LV diastolic function could be expected. The effects of fluid resuscitation from severe hemorrhagic shock with DCLHb were investigated in 20 anesthetized domestic pigs. After generation of a critical left anterior descending coronary artery stenosis (narrowing of the artery until disappearance of reactive hyperemia after a 10-second complete vessel occlusion), hemorrhagic shock (mean arterial blood pressure 45 mm Hg) was induced within 15 min by controlled blood withdrawal and maintained for 60 min. Fluid resuscitation consisted of replacement of the plasma volume withdrawn during hemorrhage by infusion of either 10% DCLHb (DCLHb group, n = 10) or 8% human serum albumin (HSA) oncotically matched to DCLHb (HSA group, n = 10). After completion of resuscitation, an observation period of 60 min elapsed. Measurements of central hemodynamics, myocardial oxygenation, and LV diastolic function were performed at baseline, after induction of critical coronary artery stenosis, after 60 min of hemorrhagic shock, immediately after resuscitation, and 60 min later. While 5 out of 10 animals treated with HSA died within the first 20 min after fluid resuscitation from acute LV pump failure, all DCLHb-treated animals survived until the end of the protocol (p < 0.05). Despite superior myocardial oxygenation due to augmentation of the arterial O(2) content as well as of coronary perfusion pressure, no beneficial effects on LV diastolic function were observed after infusion of DCLHb. Peak velocity of LV pressure decrease (dp/dt(min)) did not reveal significant differences between the two groups. Immediately after completion of fluid resuscitation with DCLHb, the time constant of LV diastolic relaxation (tau) was prolonged when compared with HSA-treated animals (p < 0.05), indicating retardation of early LV diastolic relaxation. Our data suggest that DCLHb fails to improve LV diastolic function after fluid resuscitation from severe hemorrhagic shock. However, positive effects on myocardial perfusion and oxygenation result in a significant reduction of the mortality of severe hemorrhagic shock.

Animals↗

The role of poly(ADP-ribose) polymerase activation in the development of myocardial and endothelial dysfunction in diabetes.

Patients with diabetes exhibit a high incidence of diabetic cardiomyopathy and vascular complications, which underlie the development of retinopathy, nephropathy, and neuropathy and increase the risk of hypertension, stroke, and myocardial infarction. There is emerging evidence that the activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) importantly contributes to the development of endothelial dysfunction in a streptozotocin-induced model of diabetes. We investigated the role of PARP activation in the pathogenesis of cardiac dysfunction in streptozotocin-induced and genetic (nonobese diabetic) models of diabetes in rats and mice. Development of diabetes was accompanied by hyperglycemia, cardiac PARP activation, a selective loss of endothelium-dependent vasodilation in the thoracic aorta, and an early diastolic dysfunction of the heart. Treatment with a novel potent phenanthridinone-based PARP inhibitor, PJ34, starting 1 week after the onset of diabetes, restored normal vascular responsiveness and significantly improved cardiac dysfunction, despite the persistence of severe hyperglycemia. The beneficial effect of PARP inhibition persisted even after several weeks of discontinuation of the treatment. Thus, PARP activation plays a central role in the pathogenesis of diabetic cardiovascular (cardiac as well as endothelial) dysfunction. PARP inhibitors may exert beneficial effects against the development of cardiovascular complications in diabetes.

Animals↗

Non-invasive cardiac assessment in beta-thalassaemia major.

Iron deposition in the heart occurs in beta-thalassaemia major and contributes to cardiac dysfunction. Eighteen patients with beta-thalassaemia major were assessed clinically and had non-invasive investigations. They were young (15.5 +/- 3.6 years). Two patients had clinical heart failure. Doppler echocardiography demonstrated higher transmitral peak flow velocity in early and late diastole compared with controls (e: p<0.05, a: p<0.01). Transtricuspid peak late diastolic flow velocity was higher in patients (p<0.005). Isovolumic relaxation time was shortened (p<0.001). Pulmonary venous flow velocity was higher in diastole than systole (S: 0.51 +/- 0.11 m/s, D: 0.62 +/- 0.08 m/s). Reversal of pulmonary venous flow during atrial systole was seen in eight patients. These diastolic filling abnormalities did not significantly change with blood transfusion. Left ventricular ejection fraction was normal in patients. Two patients had cardiomegaly on chest X-ray. In beta-thalassaemia with iron overload, there is a restrictive pattern of diastolic dysfunction. This is not altered by recent blood transfusion. Left ventricular function remains relatively intact.

Adolescent↗

[Doppler echocardiography for the assessment of left ventricular diastolic function: methodology, clinical and prognostic value].

To date, left ventricular diastolic function can be clinically assessed by Doppler echocardiography. The Doppler recording of mitral inflow and pulmonary venous flow provides main information about ventricular diastolic properties. At the level of the mitral inflow we can measure the early diastolic peak velocity (E), atrial peak velocity and derive their ratio, the E velocity deceleration time and isovolumic relaxation time, and calculate atrial filling fraction. At the level of the pulmonary veins, the peak systolic velocity (S), the peak diastolic velocity (D), the S/D ratio, the peak of reverse atrial velocity and its duration, above all in terms of difference with the mitral A duration, characterize the different patterns of diastolic function. Also the new ultrasound technologies are clinically useful to define ventricular diastolic properties. The myocardial early diastolic velocity (Em) detectable by pulsed tissue Doppler at the level of the mitral annulus, and the flow propagation velocity (Vp) recordable by color M-mode of left ventricular inflow, both relatively preload-independent, are measurements related to tau, the reference hemodynamic variable. The E/Em and E/Vp ratios provide accurate estimation of the changes in left ventricular end-diastolic pressure. They allow us to distinguish the pseudonormal and restrictive patterns from the normal pattern and are, therefore, alternative tools to Valsalva maneuver of mitral inflow and pulmonary venous flow. The predictive value of the pattern of abnormal relaxation (grade I of diastolic dysfunction) and both the reversible and irreversible restrictive patterns (grade III and IV respectively) is now demonstrated and permits important prognostic stratification and appropriate therapeutic management.

Diastole↗

Normalised radionuclide measures of left ventricular diastolic function.

Abnormal left ventricular diastolic function is being increasingly recognised in patients with clinical heart failure and normal systolic function. A simple routine radionuclide measure of diastolic function would therefore be useful. To establish this, the relationship of peak diastolic filling rate (normalized for either end diastolic volume, stroke volume, or peak systolic emptying rate), and heart rate, age, and left ventricular ejection fraction was studied in 64 subjects with normal cardiovascular systems using routine gated heart pool studies. The peak filling rate, when normalized to end diastolic volume, correlated significantly with heart rate, age and left ventricular ejection fraction, whereas normalization to stroke volume correlated significantly to heart rate and age but not to left ventricular ejection fraction. Peak filling rate normalized for peak systolic emptying rate correlated with age only. Multiple regression equations were determined for each of the normalized peak filling rates in order to establish normal ranges for each parameter. When using peak filling rate normalized for end diastolic volume or stroke volume, appropriate allowance must be made for heart rate, age and ejection fraction. Peak filling rate normalized to peak ejection rate is a heart rate independent parameter which allows the performance of the patient's ventricle in diastole to be compared with its systolic function. It may be used in patients with normal systolic function to serially follow diastolic function or if age corrected, to screen for diastolic dysfunction.

Adolescent↗

Color M-mode flow propagation velocity versus conventional Doppler indices in the assessment of diastolic left ventricular function in patients on chronic hemodialysis.

BACKGROUND AND OBJECTIVE: Color M-mode flow propagation velocity (Vp) has been reported as a preload-independent measure of diastolic function. To study the effects of loading conditions on diastolic function assessment in patients on chronic hemodialysis, we measured Vp and conventional Doppler indices pre- and posthemodialysis. METHODS: Twenty hemodialysis patients with normal systolic function underwent measurement of Vp, early filling velocity (E), its deceleration time (DT), atrial contraction velocity (A), isovolumic relaxation time (IVRT), and pulmonary atrial flow reversal velocity (PFR) pre- and posthemodialysis. Twelve healthy controls underwent these same measurements. RESULTS: Hemodialysis patients had significantly slower Vp at baseline than normal controls, while E/A, DT, IVRT, and pulmonary flow reversal were not significantly different. E, IVRT, and PFR were affected by hemodialysis, while color M-mode flow propagation velocities, A, and DT were not. CONCLUSION: Color M-mode flow propagation velocity seems to be a preload-independent measure of diastolic function in chronic hemodialysis patients in whom isolated diastolic dysfunction appears prevalent.

Adult↗

[The Doppler echocardiographic assessment of left ventricular diastolic function in coronary heart disease].

BACKGROUND AND OBJECTIVE: Changes in left ventricular (LV) diastolic function lead to characteristic changes in the transmitral flow profile as determined by Doppler echocardiography (DEC). Although DEC cannot provide direct quantitative measurement of LV filling pressures and is influenced by several factors, transmitral flow correlates well with LV haemodynamics. In this prospective study the results of transthoracic DEC were compared with haemodynamic parameters in patients with coronary heart disease (CHD) and their clinical value assessed. PATIENTS AND METHODS: 254 consecutive patients with CHD (67 women, 187 men, aged 62.5 +/- 8.5 years) underwent transthoracic DEC. The ratio of early to late diastolic velocity (VE/VA) and early diastolic deceleration time (DT) of the transmitral flow were measured as an indication of diastolic LV function. RESULTS: Patients with reduced LV compliance and increased filling pressure (LV end-diastolic pressure [LVEDP] > 15 mm hg) had a restrictive transmitral flow profile with a significantly higher than normal VE/VA and a shorter DT (1.35 +/- 0.84 vs. 0.86 +/- 0.26, P < 0.001; and 158 +/- 45 vs. 213 +/- 35, P < 0.001, respectively). VE/VA and DT also significantly correlated with LVEDP (r = 0.65, P < 0.001 and r = -0.60, P < 0.001 respectively). Sensitivity and specificity of an LVEDP of > 15 mm Hg were 67% and 84%, respectively, for a VE/VA of more than 1, and 65% and 91% for a DT of less than 170. The combination of the two parameters increased specificity to 97%. CONCLUSION: Determining the transmitral flow profile makes it possible noninvasively to obtain an indication of LV end-diastolic function. Patients with severe diastolic dysfunction and increased filling pressures are recognized with a high degree of specificity.

Aged↗