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Diabetic cardiomyopathy and subclinical cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis (MESA).

OBJECTIVE: Studies have demonstrated increased left ventricular mass (LVM) and diastolic dysfunction among diabetic patients without clinical cardiovascular disease (CVD), but few have assessed the potential contribution of subclinical CVD to ventricular abnormalities in diabetes. We examined whether diabetic cardiomyopathy is associated with subclinical atherosclerosis and if abnormalities are found with impaired fasting glucose (IFG). RESEARCH DESIGN AND METHODS: LVM, end-diastolic volume (EDV), and stroke volume were measured by magnetic resonance imaging (MRI), and atherosclerosis was assessed by coronary artery calcium and carotid intima-media wall thickness in 4,991 participants in the Multi-Ethnic Study of Atherosclerosis, a cohort study of adults aged 45-84 without prior CVD. Multivariable linear regression was used to analyze the association between MRI measures and glucose status. RESULTS: Increased LVM was observed in white, black, and Hispanic participants with diabetes but not among Chinese participants. After adjustment for weight, height, CVD risk factors, and subclinical atherosclerosis, ethnicity-specific differences in ventricular parameters were present. Among whites and Chinese with diabetes, LVM was similar to that in normal subjects; EDV and stroke volume were reduced. In blacks with diabetes, EDV and stroke volume were reduced, and LVM was increased (+5.6 g, P < 0.05). Among Hispanics with diabetes, EDV and stroke volume were similar to normal, but LVM was increased (+5.5 g, P < 0.05). After adjustment, IFG was associated with a decrease in EDV and stroke volume in whites and blacks only; however, no significant differences in LVM were observed. CONCLUSIONS: Ethnicity-specific differences in LVM, EDV, and stroke volume are associated with abnormal glucose metabolism and are independent of subclinical CVD.

Aged↗

Reduced compliance of left ventricle.

Diastolic function is essential for efficient systolic performance. A normal diastole allows left ventricle (LV) filling to occur under normal intracavitary pressure. It is an energy dependent process, as such affected by ischemia. Several factors influence diastolic function of the LV: the mitral valve area, the gradient between atrium and ventricle, LV relaxation and compliance, atrial compliance, the presence of sinus rhythm, the end-systolic volume. Echocardiography is the principal diagnostic tool to assess LV diastolic function noninvasively in clinical practice. Doppler evaluation allows to analyse each phase of LV diastole through measurement of transmitral and pulmonary veins flows velocities. Tissue Doppler echocardiography and color M-mode Doppler have also been introduced in the study of diastole. The use of echocardiography in the setting of diastolic dysfunction in ICU and operatory room has relevant implications in the management of haemodynamic instability, in vasoactive d rugs titration, in the detection of myocardial ischemia, and in performing prognostic stratification. These information can guide the management of cardiac patients undergoing cardiac and non cardiac surgery, in the perioperative phase, as well as in the management of critical ICU patients. On this basis evaluating the LV filling properties can contribute to improve the quality of treatments in such challenging situations.

Compliance↗

Evolving changes in Doppler mitral flow velocity pattern in rats with hypertensive hypertrophy.

OBJECTIVES: The aim of our study was to explore evolving changes in a mitral flow velocity pattern (MFVP) and its hemodynamic and pathological correlates in hypertensive rats in an isolated diastolic heart failure model. BACKGROUND: Development of left ventricular (LV) hypertrophy and concomitant diastolic dysfunction cause heart failure in hypertensive hearts even with normal systolic function; however, associated evolving change in MFVP is still unclear. METHODS: Mitral flow velocity pattern was recorded every 2 weeks from 7 to 19 weeks in six hypertensive rats. Hemodynamic and pathological correlates of Doppler mitral flow indexes were examined as an additional part of the study using the hypertensive rats at the age of 13 weeks (compensatory stage, n = 7) and at 19 weeks (heart failure stage, n = 8). RESULTS: Initial development of pressure overload LV hypertrophy resulted in a decrease in early diastolic filling wave (E), a reciprocal increase in the filling wave due to atrial contraction (A) and prolongation of deceleration time of E wave (relaxation abnormality pattern). These changes were associated with an increase in tau, an index of LV relaxation, but without a change in LV end-diastolic pressure. Transition to congestive heart failure caused an increase in E, a decrease in A and shortening of deceleration time. These changes were not associated with further increase in tau but with elevation of LV end-diastolic pressure, reflecting marked LV hypertrophy and myocardial fibrosis. CONCLUSIONS: Development of pressure overload LV hypertrophy is associated with evolving changes in MFVP from normal to relaxation abnormality pattern and, in turn, to pseudonormalized to restrictive pattern. Analysis of MFVP may be useful to follow not only functional but also constitutional changes of the myocardium in hypertensive hearts.

Animals↗

Unrecognized heart failure in elderly patients with stable chronic obstructive pulmonary disease.

AIMS: To establish the prevalence of unrecognized heart failure in elderly patients with a diagnosis of chronic obstructive pulmonary disease, in a stable phase of their disease. METHODS AND RESULTS: In a cross-sectional study, patients >/=65 years of age, classified as having chronic obstructive pulmonary disease by their general practitioner and not known with a cardiologist-confirmed diagnosis of heart failure, were invited to our out-patient clinic. Four hundred and five participants underwent an extensive diagnostic work-up, including medical history and physical examination, followed by chest radiography, electrocardiography, echocardiography, and pulmonary function tests. As reference (i.e. 'gold') standard the consensus opinion of an expert panel was used. The panel based the diagnosis of heart failure on all available results from the diagnostic assessment, guided by the diagnostic principles of the European Society of Cardiology (ESC) for heart failure (i.e., symptoms and echocardiographic systolic and/or diastolic dysfunction). The diagnosis of chronic obstructive pulmonary disease was based on the diagnostic criteria of the Global Initiative (GOLD) for chronic obstructive pulmonary disease. Of 405 participating patients with a diagnosis of chronic obstructive pulmonary disease, 83 (20.5%, 95% CI 16.7-24.8) had previously unrecognized heart failure (42 patients systolic, 41 'isolated' diastolic, and none right-sided heart failure). In total, 244 (60.2%) patients had chronic obstructive pulmonary disease according to the GOLD criteria and 50 (20.5%, 95% CI 15.6-26.1) patients combined with unrecognized heart failure. CONCLUSION: Unrecognized heart failure is very common in elderly patients with stable chronic obstructive pulmonary disease. Closer co-operation among general practitioners, pulmonologists, and cardiologists is necessary to improve detection and adequate treatment of heart failure in this large patient population.

Age Distribution↗

Intracoronary angiotensin-converting enzyme inhibition improves diastolic function in patients with hypertensive left ventricular hypertrophy.

BACKGROUND: There is increasing recognition of myocardial angiotensin-converting enzyme, which is induced with the development of left ventricular hypertrophy (LVH). The potential physiological significance of subsequent increased angiotensin I to II conversion in the presence of LVH is unclear but has been postulated to cause abnormal Ca2+ handling and secondary diastolic dysfunction. Accordingly, we hypothesized that acute angiotensin-converting enzyme inhibition would result in decreased production of angiotensin II and improved active (Ca(2+)-dependent) relaxation in patients with hypertensive LVH. METHODS AND RESULTS: Intracoronary (IC) enalaprilat was administered to 25 patients with and without LVH secondary to essential hypertension. Indexes of diastolic and systolic LV function were determined from pressure (micromanometer)-volume (conductance) analysis at steady state and with occlusion of the inferior vena cava. Patients were divided into those receiving high- (5.0 mg, n = 15) and low-dose (1.5 mg, n = 10) IC enalaprilat during a 30-minute infusion at 1 mL/min. The high-dose patients were further divided along the median normalized LV wall thickness of 0.671 cm/m2. The time constant of isovolumic relaxation (TauL) was prolonged at baseline in patients receiving high-dose enalaprilat with wall thickness > 0.671 cm/m2 (TauL, 56 +/- 2 versus 44 +/- 2 and 45 +/- 2 milliseconds, respectively, P < .01 by ANOVA) and shortened only in this patient group (TauL, 49 +/- 3 versus 46 +/- 2 and 43 +/- 2 milliseconds, respectively, P < .01 versus baseline and other groups by ANOVA). The improvement in TauL was directly proportional to the degree of LVH (r = .92, P < .001). Although there was a decrease in LV end-diastolic pressure (23 +/- 2 to 15 +/- 1 mm Hg, P < .01) and volume (86 +/- 8 to 67 +/- 9 mL/m2, P < .05) in those patients with a reduction in TauL, this is due to movement down a similar diastolic pressure-volume relation with no change in chamber elastic stiffness (0.023 +/- 0.002 to 0.025 +/- 0.004 mL-1, P = NS). CONCLUSIONS: Intracoronary enalaprilat resulted in an improvement in active (Ca(2+)-dependent) relaxation in those patients with more severe hypertensive LVH. The improvement in active relaxation was directly proportional to the severity of LVH. These results support the hypothesis that the cardiac renin-angiotensin system is an important determinant of active diastolic function in hypertensive LVH.

Adult↗

[Antiremodeling Activity of Nebivolol in Patients With Essential Hypertension and Various Types of 4a/4b Polymorphisms of Endothelial NO Synthase Gene].

Frequencies of alleles and genotypes of a polymorphic marker 4a/4b of eNOS gene and association of this marker with parameters of hemodynamics, signs of left ventricular hypertrophy and endothelial dysfunction were studied in 78 uzbek men aged 50.5+/-9.5 years with stage I-II essential hypertension. Allele 4b and genotype 4b/4b were found to be most frequent while genotypes 4a/4b and 4a/4a were associated with high degree of left ventricular hypertrophy, disturbances of 24-hour blood pressure profile and pronounced diastolic dysfunction. Three months of therapy with nebivolol exerted similar antihypertensive effect in all patients however only in patients with 4b/4b genotype it caused regression of left ventricular hypertrophy and normalization of endothelial vasoregulatory function.

Genotype↗

Myocardial damages in systemic sclerosis detected by gated myocardial perfusion SPECT and sympathetic imaging.

BACKGROUND: Cardiac involvement is an important factor for the appropriate management of systemic sclerosis (SSc). The possibility for detecting early myocardial damage was investigated using (99m)Tc methoxyisobutylisonitrile (MIBI) gated perfusion single photon emission computed tomography (SPECT) and (123)I metaiodobenzylguanidine (MIBG) sympathetic imaging. METHODS AND RESULTS: Twenty-three patients with SSc and 14 control subjects were studied. The severity of SSc was defined by disease type and semi-quantitative skin thickness scores. A myocardial perfusion study was performed using (99m)Tc MIBI exercise--rest study, and systolic and diastolic parameters were calculated from the volume curve of the gated SPECT. (123)I MIBG was evaluated by segmental defects, a heart-to-mediastinum ratio and washout rate (WR). No significant exercise-induced ischemia was observed and the left ventricular ejection fraction was within normal range in patients with SSc. However, diastolic function calculated by time to peak filling (TPF) in the early diastole was significantly prolonged in SSc compared with the control group (184+/-35 ms, 160+/-25 ms, p=0.030) and more rapid MIBG WR from the myocardium (18.2+/-7.0% vs 11.1+/-4.3%, p=0.0015). Compared with the control group, the severe group with either diffuse SSc or a skin thickness score >or=10 had more prolonged TPF/RR interval than the less severe group. Both diastolic and sympathetic abnormalities were observed in 7 (30%) patients, and 1 abnormality in 17 (74%) patients with SSc. CONCLUSIONS: In patients with SSc, either diastolic dysfunction or sympathetic derangement, or both were observed even without induced ischemia and normal ventricular contractility. Based on these subclinical early findings, further follow-up studies are recommended.

3-Iodobenzylguanidine↗

Systolic and diastolic functions in elderly patients with and without heart failure.

BACKGROUND: A considerable number of patients with heart failure (HF) have a normal left ventricular ejection fraction (LVEF). In these subjects, HF has usually been related to diastolic heart failure (DHF), still a frequently overlooked clinical entity. METHODS: This study reports the clinical, instrumental, and conventional echocardiographic evaluation of 159 consecutive, hospitalized elderly patients, 87 admitted with HF and 72 admitted for other reasons without overt HF. RESULTS: All of the 87 HF patients had signs of diastolic dysfunction (DDYS), yet 44.8% of them had a normal LVEF. Forty-four of the 72 patients admitted without overt HF (61.1%) had mild DDYS and 14 (19.5%) also had a reduced LVEF. There was a clear relationship between LVEF reduction and the severity of DDYS. CONCLUSIONS: HF is often a combination of diastolic and systolic function abnormalities. DHF may be difficult to detect in HF subjects with normal LVEF because their DDYS is often mild. However, there are signs of DDYS in all HF patients that increase in severity as LVEF decreases. DDYS could be considered a marker for all forms of HF, especially in elderly patients.

Journal Article↗

Aminoterminal pro-brain natriuretic peptide and ventricular filling pressures in heart transplant recipients.

We tested the hypothesis that, in heart transplant recipients, plasma aminoterminal pro-brain natriuretic peptide (NT-proBNP) dosage is useful for diagnosis of high ventricular loading pressures in the absence of systolic dysfunction. We studied 60 consecutive transplanted heart recipients without systolic dysfunction at 1 to 16 years after transplantation. We found that, in these patients with frequent high ventricular filling pressures, plasma NT-proBNP was highly correlated with creatininemia and not correlated with ventricular loading pressures. These results do not support the hypothesis that NT-proBNP is useful for diagnosis of isolated diastolic dysfunction in transplanted heart recipients.

Adult↗

Comparison of the effects of ACE inhibition with those of angiotensin II receptor antagonism on systolic and diastolic myocardial stunning in isolated rabbit heart.

The aim was to determine whether enalaprilat (0.08 mg/kg/min) or losartan (0.01 mg/kg/min) administration before ischemia can improve postischemic systolic and diastolic dysfunction ('stunned myocardium') and attenuate the 'hyperfunction' phase at the beginning of reperfusion. An isolated isovolumic rabbit heart preparation was subjected to 15 min of ischemia followed by 30 min of reperfusion without (group 1) or with pretreatment with enalaprilat (group 2) or losartan (group 3). Left ventricular developed pressure and end-diastolic pressure (diastolic stiffness) were measured and the time constant of isovolumic relaxation (T, Tau) and the ratio between +dP/dt and -dP/dt were calculated. In comparison to the stunned group (group 1) both enalaprilat (group 2) and losartan (group 3) exerted a significant protective effect on postischemic recovery of contractile state and diastolic stiffness. Only enalaprilat attenuated the 'hypercontractile' phase. However, both enalaprilat and losartan failed to improve myocardial relaxation. In summary, these data strongly suggest a direct deleterious action of the local renin-angiotensin system on ischemic myocardium and diminution of myocardial stunning with its successful blockade. Although, we can not exclude the possibility that bradykinin has some cardioprotective effect, these data suggest that angiotensin exacerbates myocardial injury.

Angiotensin II↗

Chronic kidney disease in patients with chronic heart failure--impact on intracardiac conduction, diastolic function and prognosis.

BACKGROUND: In patients with chronic heart failure (CHF), chronic kidney disease (CKD) is associated with increased morbidity and mortality, but contributing mechanisms are not well defined. This study tested the impact of CKD on intracardiac conduction, diastolic function and prognosis in patients with underlying CHF. METHODS: We prospectively enrolled 269 patients with stable CHF, of whom 135 had CKD (estimated glomerular filtration rate (eGFR)<60 ml/min/1.73 m(2)). Echo measurements comprised left ventricular dimensions/volumes, ejection fraction, mitral E/A-ratio, deceleration time and tissue Doppler mitral annular velocities (S', E', A'). PQ and QRS intervals were derived from the 12-lead ECG. A cardiac event (cardiac death or urgent cardiac transplantation) was defined as combined study end point. RESULTS: Patients with CKD had longer PQ and QRS intervals, and were in a poorer NYHA functional class as compared to patients without CKD. In patients with CKD, the mitral annular E' velocity was lower, the mitral E/E'-ratio was higher and a restrictive mitral filling pattern was more frequent. By linear regression analysis, PQ and QRS intervals and the mitral E/E'-ratio were inversely related to the eGFR. During a follow-up of 507+/-375 days, 39 patients suffered a cardiac event. In CKD patients, outcome was markedly poorer as compared to those without CKD (event-free survival rate 51% vs. 87% in those without KD, p=0.001) CONCLUSIONS: In patients with CHF, CKD is associated with impaired intracardiac conduction and progressive diastolic dysfunction. Both mechanisms may contribute to increased morbidity and mortality of such patients.

Age Distribution↗

Effects of dual-chamber pacing in hypertrophic cardiomyopathy on left ventricular outflow tract obstruction and on diastolic function.

Hypertrophic cardiomyopathy (HC) is characterized by impaired diastolic function and, in about 1/4 of patients, left ventricular (LV) outflow tract obstruction. Atrioventricular (AV) pacing diminishes LV outflow tract gradient in HC, but impairs diastolic function in the experimental animal and in different categories of patients. To investigate the effects of AV pacing on hemodynamics and LV function in obstructive HC, 16 patients with HC were studied by cardiac catheterization and simultaneous radionuclide angiography during atrial and AV pacing. The resting LV outflow tract gradient decreased with AV pacing from 60 +/- 34 to 38 +/- 37 mm Hg (mean +/- SD; p <0.001). Regional ejection fraction decreased significantly at the septal level from 0.81 +/- 0.21% to 0.69 +/- 0.27% (p <0.01). Pulmonary artery wedge pressure increased from 10 +/- 5 to 15 +/- 6 mm Hg (p <0.001). AV pacing induced asynchrony (i.e., the coefficient of variation of the time to end-systole increased from 7 +/- 4% to 14 +/- 10% (p <0.01). The time constant of isovolumetric relaxation (t) increased from 58 +/- 24 to 74 +/- 33 ms (p <0.02), and peak filling rate decreased from 491 +/- 221 to 416 +/- 184 ml/s (p <0.05). Thus, AV pacing greatly diminishes resting obstruction through a reduction in septal ejection fraction (i.e., an increase in LV outflow tract width in systole), but impairs active diastolic function and increases filling pressures. These latter effects are potentially detrimental in patients with HC in whom diastolic dysfunction is present.

Adult↗

Nature of heart failure in patients with ventricular septal defect.

To assess the contributions of systolic and diastolic dysfunction to congestive heart failure (CHF) in ventricular septal defect (VSD), we studied 13 children with VSD at catheterization using a Millar catheter. Eight children had CHF, whereas five did not. Phenylephrine was infused at a rate of 5 micrograms.kg-1.min-1, and M-mode echocardiography and pressure were measured simultaneously. Systolic left ventricular (LV) function was assessed by maximum LV pressure (LVP), rate of pressure development (dP/dt), and by the end-systolic pressure-diameter relation (ESPDR). Systolic myocardial function was assessed by the end-systolic stress-strain relation. Diastolic chamber function was assessed by the isovolumic relaxation time constant (tau) and by the end-diastolic pressure-diameter relation (EDPDR). Diastolic myocardial function was measured by the end-diastolic stress-strain relationship. With phenylephrine, maximum LVP increased from 99 +/- 5 to 119 +/- 4 mmHg with CHF and from 106 +/- 6 to 149 +/- 10 mmHg without CHF. +dP/dt was lower with CHF (1,582 +/- 96 mmHg/s) than without CHF (2,300 +/- 200 mmHg/s). The maximum slope of the ESPDR was 39 +/- 8 with CHF and 94 +/- 14 mmHg/cm without CHF. The maximum slope of the midwall stress-strain relation was 223 +/- 37 with CHF and 395 +/- 93 g/cm2 without CHF. tau was 25 +/- 2 without CHF compared with 32 +/- 3 ms with CHF. The EDPDR was shifted leftward with failure, whereas the stress-strain relation was similar for all patients. CHF in patients with VSD results primarily from systolic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗

Preclinical thalassemic cardiopathy: a study by acoustic densitometry.

BACKGROUND: The cardiac function in thalassemia major has never been studied at ultrasonic backscatter techniques. We assessed the utility of acoustic densitometry in thalassemic patients without clinical or echocardiographic signs of heart failure. METHODS: Three groups of subjects with comparable age, sex and body surface area were analyzed: 25 with beta-thalassemia major (group A), 14 with thalassemia intermedia (group B) and 10 healthy subjects (group C). All patients were asymptomatic and without conventional echocardiographic signs of systo-diastolic dysfunction. The left ventricular mass and volumes were echocardiographically evaluated. The ultrasonic myocardial integrated backscatter signal (IBS) was recorded and analyzed by means of acoustic densitometry in the parasternal long-axis view at the septum and posterior wall, both at the basal and intermediate levels. Both the average image intensity and the systo-diastolic variations of the IBS (cyclic variation index-CVIibs and peak-to-peak intensity-PPI), respectively related to the structure and contractility of the myocardium, were calculated. The serum ferritin and liver iron concentrations were also measured, as markers of tissue iron storage. RESULTS: The CVIibs was significantly lower in groups A and B than in group C at basal (22.7 +/- 8.4 vs 22.1 +/- 7.8 vs 31.8 +/- 10.2%; p = 0.001) and intermediate septum (24.4 +/- 7.6 vs 25.3 +/- 8.1 vs 30 +/- 9.8%; p = 0.03) and at basal (25.9 +/- 7.6 vs 24.5 +/- 6.1 vs 31.1 +/- 10.6%; p = 0.02) and intermediate posterior wall (25.1 +/- 5.1 vs 24.3 +/- 6.2 vs 30.2 +/- 6.6%; p = 0.02). The PPI was also significantly lower in groups A and B than in group C. Both CVIibs and PPI were comparable in groups A and B. The average image intensity and left ventricular mass and volumes were not significantly different in the three groups. No correlation was found between the densitometric findings and markers of tissue iron storage. CONCLUSIONS: In asymptomatic patients with thalassemia major with normal conventional indexes of systo-diastolic cardiac function, acoustic densitometry may show a reduced cyclic variation of the IBS as a possible marker of initial myocardial contractile deficiency. On the contrary, neither structural alterations nor the extent of myocardial iron stores are detectable by this technique in this type of patients.

Acoustics↗

Effect of carvedilol on diastolic function in patients with diastolic heart failure and preserved systolic function. Results of the Swedish Doppler-echocardiographic study (SWEDIC).

AIM: The purpose of this study was to investigate the effects of carvedilol on diastolic function (DF) in heart failure patients with preserved left ventricular (LV) systolic function and abnormal DF. PATIENTS AND METHODS: We randomised 113 patients with diastolic heart failure (DHF) (symptomatic, with normal systolic LV function and abnormal DF) into a double blind multi-centre study. The patients received either carvedilol or matching placebo in addition to conventional treatment. After uptitration, treatment was continued for 6 months. Two-dimensional and Doppler echocardiography were used for quantification of LV function at baseline and at follow-up. Four different DF variables were evaluated by Doppler echocardiography: mitral flow E:A ratio, deceleration time (DT), isovolumic relaxation time (IVRT) and the ratio of systolic/diastolic pulmonary venous flow velocity (pv-S/D). Primary endpoint was change in the integrated quantitative assessment of all four variables during the study. RESULTS: Ninety-seven patients completed the study. A mitral flow pattern reflecting a relaxation abnormality was recorded in 95 patients. There was no effect on the primary endpoint, although a trend towards a better effect in carvedilol treated patients was noticed in patients with heart rates above 71 beats per minute. At the end of the study, there was a statistically significant improvement in E:A ratio in patients treated with carvedilol (0.72 to 0.83) vs. placebo (0.71 to 0.76), P<0.05. CONCLUSIONS: Treatment with carvedilol resulted in a significant improvement in E:A ratio in patients with heart failure due to a LV relaxation abnormality. E:A ratio was found to be the most useful variable to identify diastolic dysfunction in this patient population. This effect was observed particularly in patients with higher heart rates at baseline.

Adrenergic beta-Antagonists↗

Aldosterone antagonist improves diastolic function in essential hypertension.

Experimental studies demonstrated that mineralocorticoid antagonists prevent or reverse myocardial fibrosis. Therefore, we tested the hypothesis that the aldosterone antagonist canrenone can improve left ventricular diastolic function in essential hypertension. Using digitized M-mode echocardiography and 24-hour blood pressure monitoring (ABPM), we realized a prospective, randomized, controlled study on 34 never-treated essential hypertensives with left ventricular diastolic dysfunction. Echocardiogram and ABPM were repeated after 6 months of effective antihypertensive treatment with ACE inhibitors and calcium antagonists (second evaluation) and then after a 6-month period with 17 patients randomly assigned to add canrenone 50 mg/d to the previous treatment (third evaluation). At the basal evaluation 32 patients had left ventricular concentric hypertrophy, and 2 patients had left ventricular concentric remodeling. All the patients had normal left ventricular systolic function. At the second evaluation blood pressure was reduced (P<0.0001), left ventricular mass index decreased (P<0.0001), and diastolic function improved (P<0.0001). After randomization, the canrenone and control groups had similar 24-hour blood pressure and left ventricular morpho-functional characteristics. At the third evaluation, despite unchanged blood pressure and similar decrease of left ventricular mass index, the canrenone group, compared with control group, showed a significantly greater increase in left ventricular diastolic indices. In essential hypertension, a low dose of aldosterone antagonist added to antihypertensive treatment significantly improved left ventricular diastolic function. This improvement, not accounted for by changes in blood pressure and left ventricular mass, can be therefore ascribed to a direct action of the drug on the myocardium.

Antihypertensive Agents↗

Effects of first myocardial infarction on left ventricular systolic and diastolic function with the use of mitral annular velocity determined by pulsed wave doppler tissue imaging.

This study was undertaken to assess the effect of a first myocardial infarction (MI) on the systolic and diastolic velocity profiles of the mitral annulus determined by pulsed wave Doppler tissue imaging and thereby evaluate left ventricular (LV) function after MI. Seventy-eight patients with a first MI were examined before discharge. Peak systolic, peak early diastolic, and peak late diastolic velocities were recorded at 4 different sites on the mitral annulus corresponding to the septum, anterior, lateral, and inferior sites of the left ventricle. In addition, the amplitude of mitral annular motion at the 4 above LV sites, the ejection fraction, and conventional Doppler diastolic parameters were recorded. Nineteen age-matched healthy subjects served as controls. Compared with healthy subjects, the MI patients had a significantly reduced peak systolic velocity at the mitral annulus, especially at the infarction sites. A relatively good linear correlation was found between the ejection fraction and the mean systolic velocity from the 4 LV sites (r = 0.74, P <.001). The correlation was also good when the mean peak systolic mitral annular velocity was tested against the magnitude of the mean mitral annular motion (r = 0.77, P <.001). When the patients were divided into 2 different groups with respect to an ejection fraction > or =0.50 or <0.50, a cutoff point of mean systolic mitral annular velocity of > or =7.5 cm/s had a sensitivity of 79% and a specificity of 88% in predicting a preserved global LV systolic function. Similar to systolic velocities, the early diastolic velocity was also reduced, especially at the infarction sites. The peak mitral annular early diastolic velocity correlated well with both LV ejection fraction (r =.66, P <.001) and mean systolic mitral annular motion (r = 0.68, P <.001). However, no correlation existed between the early diastolic velocity and conventional diastolic Doppler parameters. The reduced peak systolic mitral annular velocity seems to be an expression of regionally reduced systolic function. The peak early diastolic velocity is also reduced, especially at the infarction sites, and reflects regional diastolic dysfunction. Thus, quantification of myocardial velocity by Doppler tissue imaging opens up a new possibility of assessing LV function along its long axis.

Blood Flow Velocity↗