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PubMed2006

Left ventricular diastolic function following myocardial infarction.

An acute myocardial infarction causes a loss of contractile fibers which reduces systolic function. Parallel to the effect on systolic function, a myocardial infarction also impacts diastolic function, but this relationship is not as well understood. The two physiologic phases of diastole, active relaxation and passive filling, are both influenced by myocardial ischemia and infarction. Active relaxation is delayed following a myocardial infarction, whereas left ventricular stiffness changes depending on the extent of infarction and remodeling. Interstitial edema and fibrosis cause an increase in wall stiffness which is counteracted by dilation. The effect on diastolic function is correlated to an increased incidence of adverse outcomes. Moreover, patients with comorbid conditions that are associated with worse diastolic function tend to have more adverse outcomes after infarction. There are currently no treatments aimed specifically at treating diastolic dysfunction following a myocardial infarction, but several new drugs, including aldosterone antagonists, may offer promise.

Diastole↗
PubMed2006

Regulation of Ca2+ and Na+ in normal and failing cardiac myocytes.

Ca(2+) in cardiac myocytes regulates contractility and relaxation, and Ca(2+) and Na (+)regulation are linked via Na(+)/Ca(2+) exchange (NCX). Heart failure (HF) is accompanied by contractile dysfunction and arrhythmias, both of which may be due to altered cellular Ca(2+) handling. Smaller Ca(2+) transient and sarcoplasmic reticulum (SR) Ca(2+) content cause systolic dysfunction in HF. The reduced SR Ca(2+) content is due to: (a) reduced SR Ca(2+)-ATPase function (which also contributes to diastolic dysfunction), (b) increased expression and function of NCX (which competes with SR Ca(2+)-ATPase during relaxation, but preserves diastolic function), and (c) enhanced diastolic SR Ca(2+) leak. Relative contributions of these may vary with HF etiology and stage. Triggered arrhythmias (e.g., delayed afterdepolarizations [DADs]) are prominent in HF. DADs are due to spontaneous SR Ca(2+) release and consequent activation of transient inward NCX current, which in HF allows DADs to more readily trigger arrhythmogenic action potentials. Thus NCX and Na(+) are critical in systolic and diastolic function and arrhythmias. [Na(+)](i) is elevated in HF, which may limit SR unloading and provide some Ca(2+) influx during the HF action potential, thus limiting the depression of systolic function. High [Na(+)](i) in HF is due to enhanced Na(+) influx. Cellular Na(+)/K(+)-ATPase (NKA) function appears unaltered, despite reduced NKA expression. This dichotomy led us to test NKA regulation by phospholemman (PLM). We find that PLM regulates NKA in a manner analogous to phospholamban regulation of SR Ca(2+)-ATPase (i.e., inhibition that is relieved by PLM phosphorylation). We measured intermolecular FRET between PLM and NKA, which is reduced upon PLM phosphorylation. The lower expression level of more phosphorylated PLM in HF may explain the above dichotomy. Thus, altered Ca(2+) and Na(+) handling contributes to altered contractile function and arrhythmogenesis in HF.

Calcium↗
PubMed2005

2005 Young Investigator's Award Winner: Assessment of diastolic function in newly diagnosed hypertensives.

INTRODUCTION: The prevalence and severity of diastolic dysfunction (DD) among newly diagnosed hypertensives (NDHT) is not fully established. The aim of this study was to evaluate left ventricular diastolic function (LVDF) in patients with NDHT. MATERIALS AND METHODS: This study involved 396 subjects (198 NDHT, age and gender matched 198 normotensives; age, 30 to 50 years). Parameters of LVDF included Doppler-echocardiographic measurements of peak early (E) and late (A) diastolic velocities, E-wave deceleration time (DT) and isovolumetric relaxation time (IVRT). E/A ratio of <1 was taken as an indicative of DD. RESULTS: Patients with NDHT had reduced E/A ratio (1.27 +/- 0.41 vs 1.37 +/- 0.35, P <0.001) and shortened DT (180.0 +/- 40.0 ms vs 190.0 +/- 30.0 ms, P = 0.025). The peak A velocity and IVRT were increased in the NDHT group [(62.73 +/- 13.82 ms vs 58.26 +/- 12.40 ms, P = 0.002) and (90.0 +/- 20.0 ms vs 80.0 +/- 10.0 ms, P <0.001), respectively]. Peak E velocity was similar in both groups. The prevalence of DD was increased in the NDHT group, 18.6% (32) vs 3.4% (6), P <0.001. Of the 32 NDHT subjects who had DD, 84.4% (27) had no left ventricular hypertrophy (LVH) and 15.7% (5) had LVH. Diastolic function was negatively correlated with age, body mass index, systolic blood pressure, diastolic blood pressure and left ventricular mass index. CONCLUSION: Impairment in LVDF occurs in NDHT which may precede structural abnormalities. Hypertension, obesity, older age and LVH are associated with worsening of diastolic function.

Adult↗
PubMed2005

Sprint training improves postischemic, left ventricular diastolic performance.

We examined the effects of sprint training on left ventricular diastolic stiffness during normoxia and after ischemia-reperfusion (I/R). Thirty-seven, male Sprague-Dawley rats, weighing 150-175 g at the initiation of the experiment, were randomly assigned to a sedentary, control group (n = 20) or to a high-intensity, sprint-trained group (n = 17). Animals were trained 5 days/wk on a motor-driven treadmill for 6 wk. High-intensity sprint training consisted of running five 1-min sprints at 75 m/min, 15% grade, interspersed with 1-min active recovery runs at a speed of 20 m/min, 15% grade. Langendorff-derived isolated heart performance was measured before and after 20 min of no-flow ischemia followed by 30 min of reperfusion. Isolated myocytes were harvested from a subset of postischemic hearts. Sprint training reduced Langendorff-derived LV chamber stiffness (P < 0.05) and induced a rightward shift in the LV pressure-volume relationship during both normoxic perfusion and after I/R. LV developed pressure after I/R was also better preserved in hearts obtained from sprint-trained animals (P < 0.05), a result that is in part related to a lower postischemic LV chamber stiffness in sprint-trained hearts. The putative impact of sprint training on postischemic LV chamber stiffness was masked by glycolytic inhibition with iodoacetate, suggesting that glycolysis was involved in the better postischemic recovery observed in sprint-trained hearts. There was a tendency for enhanced postischemic cardiomyocyte shortening in sprint-trained cardiomyocytes compared with control. The rate of myocyte relaxation, i.e., time for 50% relaxation of the Ca(2+) transient amplitude, was similar between groups. These data suggest that additional mechanisms unrelated to Ca(2+) were involved in sprint-induced protection from ischemia-reperfusion-induced LV diastolic dysfunction.

Animals↗
PubMed2001

[Disorders of diastolic function in patients on hemodialysis].

INTRODUCTION: Impaired cardiac function is frequently present in patients on maintenance haemodialysis. AIM: To assess the left ventricular diastolic function in patients on haemodialysis. MATERIAL AND METHODS: We used 2D and pulsed wave Doppler echocardiography to evaluate the left ventricular diastolic function in 40 patients on haemodialysis and compared those to healthy controls. RESULTS: Majority of Doppler parameters were changed in patients on haemodialysis. Diastolic dysfunction was present in 77.5% patients. In comparison to the healthy controls haemodialysis patients showed significant increase in peak velocity of late diastolic filling, (A wave, 76.82 +/- 23.76 cm/s vs. 58.46 +/- 9.65 cm/s p < 0.001) and reduction in the E/A ratio (1.00 +/- 0.26 vs. 1.26 +/- 0.31 p < 0.001). CONCLUSION: There was significant impairment in left ventricular diastolic function in patients on haemodialysis.

Diastole↗
PubMedDate not supplied

Management of heart failure and coronary artery disease in patients with chronic kidney disease.

Cardiovascular disease (CVD) is a major contributor to the mortality and morbidity of patients who suffer from chronic kidney disease (CKD). Heart failure and ischemic heart disease (IHD) are both highly prevalent in this population. The diagnosis of myocardial dysfunction is usually based on echocardiography. As in the general population, systolic dysfunction is treated with a combination of diuretics, renin-angiotensin system blockade, and beta-receptor antagonists. Diastolic dysfunction is best managed by eliminating the cause. Non-invasive tests for coronary artery disease (CAD) may be less reliable in patients with renal disease compared with nonuremic patients. Medical therapy of IHD in this population is generally similar to that for other patient groups, but surgical revascularization appears to carry a higher risk of complications with poorer clinical outcomes. The choice of revascularization procedure (coronary artery bypass grafting versus percutaneous transluminal angioplasty) should be based on the specific coronary anatomy of a given patient as well as a consideration of other comorbid factors.

Angioplasty, Balloon, Coronary↗
PubMed1993

Amrinone enhances myocardial contractility and improves left ventricular diastolic function in conscious and anesthetized chronically instrumented dogs.

BACKGROUND: Volatile anesthetics depress left ventricular mechanical performance in vivo by altering intracellular calcium regulation. Although amrinone has been shown to reverse the negative inotropic effects of volatile anesthetics, the actions of amrinone on anesthetic-induced diastolic dysfunction are unknown. This investigation examined and compared the direct effects of amrinone on left ventricular systolic and diastolic function in conscious and anesthetized dogs. METHODS: Experiments were conducted in the presence of pharmacologic blockade of the autonomic nervous system, because autonomic activity may influence the hemodynamic actions of volatile anesthetics and amrinone in vivo. Three groups, comprising a total of 27 experiments, were conducted using 9 dogs chronically instrumented for measurement of aortic and left ventricular pressure, left ventricular dP/dt, subendocardial segment length, diastolic coronary blood flow velocity, and cardiac output. Myocardial contractility was evaluated using the preload recruitable stroke work relationship slope (Mw). Diastolic function was characterized by a time constant of isovolumic relaxation (tau), a regional chamber stiffness constant (KT), and maximum segment lengthening velocity during rapid ventricular filling (dL/dtmax). On three separate days, an amrinone bolus of 1 mg/kg, followed by an infusion at 10, 20, 40, or 80 micrograms.kg-1.min-1, was administered. Hemodynamics and ventricular pressure-segment length loops and waveforms were recorded after a 15-min equilibration at each dose in the conscious state or during isoflurane or halothane anesthesia (1.25 MAC). RESULTS: In conscious dogs, amrinone significantly increased myocardial contractility in a dose-dependent manner (Mw of 65 +/- 8 to 108 +/- 10 mmHg at the high dose). Amrinone also shortened isovolumic relaxation (tau of 32.7 +/- 2.1 to 24.8 +/- 0.9 ms at the high dose) and enhanced rapid ventricular filling (dL/dtmax of 34.8 +/- 1.2 to 45.1 +/- 2.3 mm/s at the high dose) in a dose-related fashion. In addition, amrinone reduced regional chamber stiffness (Kp of 0.49 +/- 0.09 to 0.31 +/- 0.08 mm/s at the high dose) in conscious dogs. Amrinone also enhanced left ventricular systolic (increase in Mw) and diastolic function (decreases in tau and Kp and increases in dL/dtmax) when this drug was administered to dogs anesthetized with isoflurane or halothane. CONCLUSIONS: Amrinone produced positive inotropic and lusitropic effects in both conscious and anesthetized dogs with autonomic nervous system blockade. These results indicate that amrinone-induced improvement of left ventricular performance are related to actions in diastole, as well as systole.

Amrinone↗
PubMed2004

Abnormal diastolic flow demonstrated by color M mode echocardiography in hypertrophic cardiomyopathy with mid-ventricular cavity obliteration.

We report a case of a 55-year-old woman who presented with ventricular tachycardia and myocardial infarction. Investigations revealed no disease of the epicardial coronary arteries, but a diagnosis of hypertrophic cardiomyopathy with mid-cavitary dynamic obstruction was made. Detailed echocardiographic examination, including pulse-wave Doppler and Color M Mode recordings revealed unusual components of diastolic dysfunction.

Blood Flow Velocity↗
PubMed1989

Left ventricular function in beta thalassaemia major.

The left ventricular dimension and posterior wall dynamics were studied by computer assisted analysis of M mode echocardiography in 25 normal children (group 1) and 32 transfusion dependent children with beta thalassaemia major who had no evidence of heart failure (group 2). Twenty seven of those in group 2 remained well but five died of cardiac decompensation within 12 months. Compared with group 1, the left ventricular fractional shortening and ejection fraction were normal in those in group 2 who survived but diminished in those who died. Evaluation of left ventricular dimension and posterior wall dynamics during systole (peak shortening rate, peak velocity of circumferential fibre shortening, and peak posterior wall thickening rate) showed similar findings in that only the group who died had abnormal values. The left ventricular dimension and posterior wall diastolic dynamics (peak relaxation rate, normalised peak relaxation, peak wall thinning, and normalised peak wall thinning rate), however, showed progressively slower rates in all the children in group 2. The findings suggest that left ventricular diastolic dysfunction occurs early in myocardial impairment in patients with beta thalassaemia major. When there are abnormalities in both diastole and systole, the myocardial impairment is advanced and the prognosis is poor.

Adolescent↗
PubMed2006

[Evaluation of diastolic function during and post-exercise in patients with arterial hypertension].

UNLABELLED: It is known that patients with arterial hypertension and ventricular hypertrophy have diastolic alterations, in particular during exercise. However, it is controversial if diastolic dysfunction continues once exercise had concluded. The objective was to assess the effects of isometric exercise on the diastolic function in patients with arterial hypertension. Five control patients (group 1, G1) and 7 patients with arterial hypertension (group 2, G2) were studied. All patients underwent cardiac catheterization and performed isometric exercise until heart rate increased 43 +/- 7%. Left ventricular systolic pressure (LVSP) and end diastolic pressure (LVEDP) were measured. We calculated, +dP/dt(max), the time constant of isovolumic pressure decay (tau) and t1/2 were all measured. RESULTS: The LVSP increased in G1 and G2 during exercise from 140 +/- 3 to 195 +/- 14 mm Hg (p < 0.05) and 161 +/- 9 to 238 +/- 15 mm Hg, respectively; returning to their basal values once exercise had concluded. The tau (tau) and t1/2 increased, while exercising in G2, from 23 +/- 2 and 15 +/- 2 msec to 35 +/- 7 and 23 +/- 4 msec, respectively. After exercise both variables continued elevated reaching 41 +/- 6 msec (p < 0.05) and 23 +/- 3 msec (p < 0.05), respectively. In conclusion, isometric exercise decreases relaxation rate and increases LVEDP in patients with arterial hypertension and ventricular hypertrophy. After exercise, isovolumic relaxation remained altered suggesting the presence of stunned myocardium.

Aged↗
PubMed1996

[Restrictive myocardiopathy in children. A study of 4 patients].

Restrictive cardiomyopathy is an unusual form of cardiomyopathy during childhood. Only occasional cases or reduced populations have been reported in international journals. The purpose of this report is to document the clinical, echocardiographic and hemodynamic profile and outcome of restrictive cardiomyopathy in a group of four children (two boys and two girls). The mean age at admission was 3.5 +/- 2.7 years (range 1(3/12) to 7(10/12) years). The diagnosis was made by clinical, echocardiographic and hemodynamic criteria. The main symptoms were bronchial disease (two patients), hepatomegaly and a cardiac murmur. All of the patients had impaired growth and physical development, normal or near-normal Rx cardiothoracic ratio, evidence of congestive heart failure and only one of them showed a cardiac murmur. The most common ECG finding was biatrial enlargement and incomplete right-bundle branch block. The echocardiographic feature was severe biatrial dilatation in the presence of normal ventricular cavity size. Left ventricular shortening was normal and there was diastolic dysfunction. Doppler mitral flow was restrictive, with an E/A ration > 1.5. Marked elevation of left ventricular end-diastolic pressure was noted in cardiac catheterization (x = 32 +/- 7 mmHg). Right ventricular end-diastolic pressure was elevated, but less than the left side (x = 19 +/- 12 mmHg). The outcome was very poor. Two patients died, one remains with heart failure NYHA II and the other with heart failure NYHA IV. We conclude that restrictive cardiomyopathy during childhood may simulate a bronchial or liver disease, so we must bear this in mind in order to make the differential diagnosis. Because of the poor prognosis and lack of specific treatment, the best therapeutic option may be heart transplantation.

Cardiomyopathy, Restrictive↗
PubMed1994

[Change in right ventricular diastolic function in children and adolescents with mucoviscidosis--a Doppler echocardiographic study].

The present study investigated the right ventricular filling pattern with Dopplerechocardiography in childhood and adolescent patients (n = 31) with cystic fibrosis and in normal subjects. The results show that, as the pulmonary pressure increases (RPEP/AT > or = 1.0), the peak flow velocity during atrial contraction and the triangle under the atrial velocity are significantly increased while the acceleration half-time is significantly decreased. These are sensitive parameters for right ventricular diastolic dysfunction.

Adolescent↗
PubMed1996

Newer Doppler measures of left ventricular diastolic function.

Left ventricular (LV) diastolic dysfunction is an important cause of heart failure, and recent advances in the application of Doppler techniques allow a semiquantitative assessment of LV diastolic performance. This review discusses the use of Doppler echocardiography in the comprehensive assessment of LV diastolic function and performance in terms of the normal mitral and pulmonary venous flow profiles, their physiologic basis, and alterations in diseased states. There is also a discussion on the newer aspects of mitral flows such as relative durations of mitral A and pulmonary vein AR waves, E- and A- wave propagation inside the LV with their hemodynamic correlates, and derivation of ventricular dP/dt and Tau from the mitral regurgitation velocity profile. Analysis of these flow profiles and the other Doppler measures alluded to above allow one to make a fairly precise hemodynamic assessment of a patient in terms of left atrial pressure, LV relaxation and stiffness and the profile of LV diastolic pressure in terms of pre- 'a' wave and 'a' wave pressures and ventricular end-diastolic pressure.

Echocardiography, Doppler↗
PubMed1999

The value of assessing pulmonary venous flow velocity for predicting severity of mitral regurgitation: A quantitative assessment integrating left ventricular function.

Although alteration in pulmonary venous flow has been reported to relate to mitral regurgitant severity, it is also known to vary with left ventricular (LV) systolic and diastolic dysfunction. There are few data relating pulmonary venous flow to quantitative indexes of mitral regurgitation (MR). The object of this study was to assess quantitatively the accuracy of pulmonary venous flow for predicting MR severity by using transesophageal echocardiographic measurement in patients with variable LV dysfunction. This study consisted of 73 patients undergoing heart surgery with mild to severe MR. Regurgitant orifice area (ROA), regurgitant stroke volume (RSV), and regurgitant fraction (RF) were obtained by quantitative transesophageal echocardiography and proximal isovelocity surface area. Both left and right upper pulmonary venous flow velocities were recorded and their patterns classified by the ratio of systolic to diastolic velocity: normal (>/=1), blunted (<1), and systolic reversal (<0). Twenty-three percent of patients had discordant patterns between the left and right veins. When the most abnormal patterns either in the left or right vein were used for analysis, the ratio of peak systolic to diastolic flow velocity was negatively correlated with ROA (r = -0.74, P <.001), RSV (r = -0.70, P <.001), and RF (r = -0.66, P <.001) calculated by the Doppler thermodilution method; values were r = -0.70, r = -0.67, and r = -0.57, respectively (all P <.001), for indexes calculated by the proximal isovelocity surface area method. The sensitivity, specificity, and predictive values of the reversed pulmonary venous flow pattern for detecting a large ROA (>0.3 cm(2)) were 69%, 98%, and 97%, respectively. The sensitivity, specificity, and predictive values of the normal pulmonary venous flow pattern for detecting a small ROA (<0.3 cm(2)) were 60%, 96%, and 94%, respectively. However, the blunted pattern had low sensitivity (22%), specificity (61%), and predictive values (30%) for detecting ROA of greater than 0.3 cm(2) with significant overlap with the reversed and normal patterns. Among patients with the blunted pattern, the correlation between the systolic to diastolic velocity ratio was worse in those with LV dysfunction (ejection fraction <50%, r = 0.23, P >.05) than in those with normal LV function (r = -0.57, P <.05). Stepwise linear regression analysis showed that the peak systolic to diastolic velocity ratio was independently correlated with RF (P <.001) and effective stroke volume (P <.01), with a multiple correlation coefficient of 0.71 (P <.001). In conclusion, reversed pulmonary venous flow in systole is a highly specific and reliable marker of moderately severe or severe MR with an ROA greater than 0.3 cm(2), whereas the normal pattern accurately predicts mild to moderate MR. Blunted pulmonary venous flow can be seen in all grades of MR with low predictive value for severity of MR, especially in the presence of LV dysfunction. The blunted pulmonary venous flow pattern must therefore be interpreted cautiously in clinical practice as a marker for severity of MR.

Aged↗
PubMed2006

Early diastolic impairment of diabetic heart: the significance of right ventricle.

BACKGROUND: Left ventricular diastolic dysfunction represents the earliest preclinical manifestation of diabetic cardiomyopathy. Right ventricular function has not been studied in depth yet in diabetic patients, although the right ventricle has an important contribution to the overall cardiac function. This study was designed to assess diastolic and systolic ventricular function in both ventricles, in patients with type 1 diabetes, free from coronary artery disease and hypertension. METHODS: We studied 66 type 1 diabetic patients and 66 age- and sex-matched normal subjects by conventional and tissue Doppler echocardiography. A possible correlation was examined for age, diabetes duration and echocardiographic measurements of left ventricular and right ventricular functions with univariate analysis. RESULTS: Type 1 diabetic patients were found to have impaired diastolic function in both ventricles with either conventional or tissue Doppler echocardiography. On the contrary, systolic function in both ventricles was preserved in our diabetic population. The measured indexes showed an expected correlation with age and diabetes duration except from systolic velocity in tricuspid annulus determined by color tissue Doppler. Moreover, significant correlations were found among parameters of left and right ventricular function. CONCLUSIONS: Patients with type 1 diabetes mellitus have impaired diastolic function, and particularly relaxation, in both ventricles before the development of myocardial systolic dysfunction. These alterations in myocardial function may be attributed to ventricular interdependence as well as to the uniform effect of diabetes to cardiac function.

Adult↗
PubMed1995

Abnormal left ventricular diastolic function during cold pressor test in uncomplicated insulin-dependent diabetes mellitus.

1. Insulin-dependent diabetes mellitus is a known risk factor for congestive heart failure and an early diastolic dysfunction has been described. In order to see if diabetes itself and not complications like hypertension, nephropathy or ischaemic heart disease can be considered responsible for the abnormal diastolic function of the left ventricle, 17 young patients with uncomplicated insulin-dependent diabetes mellitus and 12 control subjects were exposed to a cold pressor test. 2. Blinded echo-Doppler examination was performed before and during the test. During basal conditions, left ventricular dimensions and volumes were smaller in diabetes and atrial contributions to left ventricular filling were increased. 3. During the cold pressor test, isovolumic relaxation time increased, peak early filling velocity (E) decreased, E deceleration time decreased and atrial contribution (A) increased significantly in diabetes, while only A increased in the control group. A marked increase in left atrial ejection force was seen in diabetes only (P < 0.002). This difference was seen in spite of comparable reductions in mitral area and atrioventricular compliance in the two groups. 4. The hyperfunction of the left atrium in diabetes is hypothesized to be due to reduce size of the left ventricle combined with incipient autonomic neuropathy.

Adolescent↗
PubMed1997

[Recovery process from myocardial stunning after transient ischemia: assessment with pulsed wave Doppler transmitral flow pattern].

Sustained left ventricular systolic dysfunction after transient myocardial ischemia is well known as "myocardial stunning", but little is known about the recovery in left ventricular diastolic function. Changes in left ventricular systolic and diastolic performance following dobutamine-induced ischemia were investigated in 13 patients with chest pain syndrome and normal coronary arteries (control) and 34 patients with coronary artery disease. Two-dimensional echocardiography and pulsed wave Doppler transmitral flow velocity curves were recorded at baseline, after infusion of a peak dose of dobutamine and at 20 min and 2 hours after dobutamine infusion. In control subjects, left ventricular ejection fraction and the peak early diastolic filling velocity increased at the peak dose of dobutamine. At 20 min after the cessation of dobutamine infusion, these values were restored to the baseline levels. In patients with coronary artery disease, ejection fraction and peak velocity increased at the peak dose of dobutamine but decreased at 20 min after infusion compared with baseline values despite the restoration of heart rate and blood pressure. Although ejection fraction increased at 2 hours compared with 20 min after infusion, peak velocity did not increase. Left ventricular diastolic dysfunction may be sustained longer than systolic dysfunction after transient myocardial ischemia.

Aged↗
PubMed1990

Progress in cardioprotection: the role of calcium antagonists.

Calcium antagonists are now widely used for the treatment of clinical hypertension and angina pectoris. They are efficacious for the treatment of vasospastic, fixed atherosclerotic and mixed angina; they reduce the incidence of silent ischemia; and they have been shown to reduce postmyocardial infarct angina. Experimental data suggest that they may have certain cardioprotective properties in cases of acute myocardial ischemia and infarction, stunned myocardium, diastolic dysfunction, left ventricular hypertrophy and atherosclerosis. Moreover, they have been shown to improve exercise performance, as well as the diastolic abnormalities in patients with hypertrophic cardiomyopathy. In animals, they may delay or reduce the extent of myocardial necrosis after coronary occlusion or coronary occlusion followed by reperfusion, and in low doses that do not alter the hemodynamic profile, they have been shown to enhance the return of ventricular function in animals with stunned myocardium. However, the early first-generation calcium antagonists (nifedipine, verapamil, diltiazem) have not been shown to reduce myocardial infarct size or to enhance survival in patients with acute myocardial infarction. There now are clinical studies that suggest that, unlike beta blockers or nitrates, nifedipine may slow the development of atherosclerotic progression in humans over a 2-year period, and it seems likely that in the 1990s there will be further expansion of the use of calcium antagonists for not only angina and hypertension but also for aspects of cardioprotection. That calcium antagonists may delay, prevent or possibly regress atherosclerotic lesions is an exciting possibility.

Amlodipine↗