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PubMed1998

Long acting calcium antagonist amlodipine prevents left ventricular remodeling after myocardial infarction in rats.

OBJECTIVE: The purpose of this study was to examine the effect of amlodipine, a long-acting calcium antagonist, on the left ventricular remodeling, including systolic and diastolic dysfunction, the change of cardiac gene expression in the myocardial infarcted rats (MI). METHODS: On the first day after myocardial infarction, the animals were randomly assigned to amlodipine treatment (n = 8) or untreated groups (MI; n = 9). We then performed Doppler-echocardiographic examinations and measured the hemodynamics at four weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. RESULTS: Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 22 +/- 1 mmHg and 5 +/- 1 mmHg. Amlodipine reduced LVEDP and CVP to 15 +/- 1 mmHg (P < 0.01) and 3 +/- 0 mmHg (P < 0.01). The weight of right ventricle in MI was significantly larger than in the control rats (Control; 0.48 +/- 0.01 g/kg, MI; 0.79 +/- 0.04 g/kg, P < 0.01). Left ventricular end-diastolic dimension (LVDd) in MI increased to 10.3 +/- 0.3 mm (P < 0.01) (Control; 6.2 +/- 0.3 mm). Amlodipine prevented an increase of the weight of right ventricle (0.62 +/- 0.03 g/kg, P < 0.01) and LVDd (7.9 +/- 0.2 mm, P < 0.01 to MI). The rats in MI showed systolic dysfunction shown by the decreased fractional shortening (Control; 31 +/- 2% versus MI; 15 +/- 1%, P < 0.01), and diastolic dysfunction shown by E wave deceleration rate (Control; 18.1 +/- 2.0 m/s2, MI; 32.6 +/- 2.1 m/s2, P < 0.01). Amlodipine significantly prevented systolic and diastolic dysfunction. The increases in beta-MHC, alpha-skeletal actin, and ANP mRNAs in the non-infarcted left ventricle and right ventricle at four weeks after the myocardial infarction were all significantly suppressed by the treatment with amlodipine. On the other hand, depressed alpha-MHC was restored to normal levels by amlodipine in both regions. CONCLUSIONS: Amlodipine prevents the left ventricular remodeling process accompanied by systolic and diastolic dysfunction, and inhibits abnormal cardiac gene expression after myocardial infarction.

Actins↗
PubMed1992

Expression of dihydropyridine receptor (Ca2+ channel) and calsequestrin genes in the myocardium of patients with end-stage heart failure.

Cytoplasmic free calcium ions (Ca2+) play a central role in excitation-contraction coupling of cardiac muscle. Abnormal Ca2+ handling has been implicated in systolic and diastolic dysfunction in patients with end-stage heart failure. The current study tests the hypothesis that expression of genes encoding proteins regulating myocardial Ca2+ homeostasis is altered in human heart failure. We analyzed RNA isolated from the left ventricular (LV) myocardium of 30 cardiac transplant recipients with end-stage heart failure (HF) and five organ donors (normal control), using cDNA probes specific for the cardiac dihydropyridine (DHP) receptor (the alpha 1 subunit of the DHP-sensitive Ca2+ channel) and cardiac calsequestrin of sarcoplasmic reticulum (SR). In addition, abundance of DHP binding sites was assessed by ligand binding techniques (n = 6 each for the patients and normal controls). There was no difference in the level of cardiac calsequestrin mRNA between the HF patients and normal controls. In contrast, the level of mRNA encoding the DHP receptor was decreased by 47% (P less than 0.001) in the LV myocardium from the patients with HF compared to the normal controls. The number of DHP binding sites was decreased by 35-48%. As reported previously, expression of the SR Ca(2+)-ATPase mRNA was also diminished by 50% (P less than 0.001) in the HF group. These data suggest that expression of the genes encoding the cardiac DHP receptor and SR Ca(2+)-ATPase is reduced in the LV myocardium from patients with HF. Altered expression of these genes may be related to abnormal Ca2+ handling in the failing myocardium, contributing to LV systolic and diastolic dysfunction in patients with end-stage heart failure.

Adolescent↗
PubMed2003

Sarcoplasmic reticulum calcium defect in Ras-induced hypertrophic cardiomyopathy heart.

The small G protein Ras-mediated signaling pathway has been implicated in the development of hypertrophy and diastolic dysfunction in the heart. Earlier cellular studies have suggested that the Ras pathway is responsible for reduced L-type calcium channel current and sarcoplasmic reticulum (SR) calcium uptake associated with sarcomere disorganization in neonatal cardiomyocytes. In the present study, we investigated the in vivo effects of Ras activation on cellular calcium handling and sarcomere organization in adult ventricular myocytes using a newly established transgenic mouse model with targeted expression of the H-Ras-v12 mutant. The transgenic hearts expressing activated Ras developed significant hypertrophy and postnatal lethal heart failure. In adult ventricular myocytes isolated from the transgenic hearts, the calcium transient was significantly depressed but membrane L-type calcium current was unchanged compared with control littermates. The expressions of sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA)2a and phospholamban (PLB) were significantly reduced at mRNA levels. The amount of SERCA2a protein was also modestly reduced. However, the expression of PLB protein and gross sarcomere organization remained unchanged in the hypertrophic Ras hearts, whereas Ser(16) phosphorylation of PLB was dramatically inhibited in the Ras transgenic hearts compared with controls. Hypophosphorylation of PLB was also associated with a significant induction of protein phosphatase 1 expression. Therefore, our results from this in vivo model system suggest that Ras-induced contractile defects do not involve decreased L-type calcium channel activities or disruption of sarcomere structure. Rather, suppressed SR calcium uptake due to reduced SERCA2a expression and hypophosphorylation of PLB due to changes in protein phosphatase expression may play important roles in the diastolic dysfunction of Ras-mediated hypertrophic cardiomyopathy.

Animals↗
PubMed2000

Decreased left ventricular contractility reserve in patients with never-treated essential hypertension.

1. Left ventricular diastolic dysfunction is often present in patients with essential hypertension. To determine whether left ventricular systolic function is normal or subnormal, we evaluated the global left ventricular contractile reserve in patients with untreated essential hypertension. 2. Thirty-one untreated men with essential hypertension and 12 normotensive healthy men were evaluated. Hypertensives were divided into two groups based on the presence (group Hc; n = 21) or absence (group Hn; n = 10) of concentric left ventricular geometric remodelling, which was defined as a relative wall thickness > or = 0.45 on M-mode echocardiography. We compared echocardiographic data of left ventricular function in hypertensive men with those in healthy men under beta-adrenoreceptor activation by up to 10 microg/kg per min dobutamine infusion. 3. At baseline, endocardial (eFS) and midwall fractional shortening of the left ventricle, the early peak filling velocity (E), the peak late filling velocity (A) and the ratio E/A were similar in the three groups. During dobutamine infusion, eFS was significantly lower in groups Hc and Hn (54.1+/-9.2 and 54.1+/-7.9%, respectively) than that observed in group N (61.7+/-7.4%). In addition, eFS was highly correlated with circumferential end-systolic wall stress (ESS) during dobutamine infusion in the three groups. In 11 subjects in group Hc (52%), the eFS-ESS relationship was lower than the 95% confidence limit of the normal regression. Comparing group Hc with groups N and Hn, it was found that E (0.52+/-0.12, 0.71+/-0.16 and 0.63+/-0.15 m/s, respectively) and E/A (0.74+/-0.23, 1.24+/-0.53 and 0.98+/-0.37, respectively) were significantly lower. 4. Our results suggest that, in addition to diastolic dysfunction, the reserve of systolic function decreased under beta-adrenoceptor activation in patients with essential hypertension.

Adrenergic beta-Agonists↗
PubMed1995

Cell geometry and contractile abnormalities of myocytes from failing human left ventricle.

OBJECTIVES: Systolic and diastolic dysfunction of the failing human heart may be due to changes in myocyte function, or to extracellular influences such as necrosis, fibrosis or repositioning of viable cells. In order to determine the contribution of cellular factors we have characterised the contraction amplitudes, and contraction and relaxation velocities of single myocytes isolated from failing human left ventricle. METHODS: Myocytes were enzymatically isolated from the left ventricles of 42 subjects, superfused at 32 degrees C and paced at 0.2 Hz. Using a video/edge tracking system we obtained contraction amplitude and contraction and relaxation velocities as well as times to peak contraction (TTP) and to 50% and 90% relaxation (R50 and R90). Concentration-response curves to Ca2+ were constructed for each cell. RESULTS: There was little difference in contraction amplitude at any Ca2+ concentration between cells from failing and non-failing hearts at this low frequency. At maximally activating Ca2+ concentrations (6-20 mM) there was a 30% slowing of relaxation velocity in myocytes from patients with both mild-moderate (P < 0.001) and severe (P < 0.001) congestive heart failure. Contraction and relaxation times were increased in myocytes from failing hearts [TTP: 0.46 +/- 0.02 s (n = 34 patients) vs. 0.35 +/- 0.02 s (n = 6), P < 0.01 and R50: 0.25 +/- 0.02 s (n = 34) vs. 0.16 +/- 0.02 s (n = 6), P < 0.001]. Impaired relaxation was seen with most etiologies, including ischemic and dilated cardiomyopathies and mitral valve disease. Myocytes from failing hypertrophied ventricles were more severely affected than those from failing non-hypertrophied hearts for both contraction and relaxation velocities. Cells from failing hypertrophied ventricles had a significantly larger area than from non-failing or failing non-hypertrophied ventricles, although cell length and sarcomere length were similar between groups. Larger myocytes did not show a more pronounced change in relaxation velocity than normally sized cells from the same hypertrophied ventricle. CONCLUSIONS: Significant impairment of relaxation can be observed in ventricular myocytes from failing human heart under conditions where contraction amplitude appears normal. The defect is not confined to one etiology of disease, but is exacerbated during hypertrophy. An increase in cell size, although observed in myocytes from hypertrophied ventricle, does not itself account for changes in relaxation. Cellular changes contribute to diastolic dysfunction in the failing human heart.

Adolescent↗
PubMed2001

Doppler echocardiography-derived index of myocardial performance (TEI index): comparison with brain natriuretic peptide levels in various heart disease.

Plasma brain natriuretic peptide (BNP) has diagnostic and prognostic value in heart failure. Cardiac dysfunction varies from systolic or diastolic dysfunction alone to the combination of both. In the present study, Doppler echocardiographic parameters, including the Doppler echocardiography-derived index (TEI index), were compared with plasma BNP levels in 74 patients with various heart diseases. Blood sampling was performed before an echocardiographic examination was conducted. The TEI index was defined as the summation of isovolumic contraction and relaxation time divided by ejection time. In patients with left ventricular (LV) systolic dysfunction (ejection fraction <50%), the TEI index and BNP were increased significantly compared with patients with normal LV systolic function (p<0.05). Patients with a TEI index > or =0.45 showed significantly increased BNP levels compared with patients with a TEI index <0.45, irrespective of LV systolic function (241.4+/-451.2 vs 65.9+/-81.8pg/ml; p<0.05). The TEI index was significantly higher in patients with a BNP > or =73pg/ml than in patients with BNP <73pg/ml (0.57+/-0.24 vs 0.46+/-0.17; p<0.05). Other echocardiographic parameters did not correlate significantly with levels of plasma BNP. Of the echocardiographic parameters, a simple Doppler index (TEI index) that combines systolic and diastolic function can detect LV dysfunction in patients with high levels of plasma BNP in various heart diseases.

Adolescent↗
PubMed1996

The role of hypertension in the pathogenesis of heart failure. A clinical mechanistic overview.

Hypertension plays a key role in the evolution of the syndrome of heart failure. Hypertension has been identified as the chief precursor of left ventricular hypertrophy. Hypertensive left ventricular hypertrophy can lead to ventricular diastolic dysfunction; it is also a risk factor for myocardial infarction, which is a principal cause of left ventricular systolic dysfunction. Asymptomatic left ventricular dysfunction, whether systolic or diastolic, culminates in clinically overt heart failure when a threshold is exceeded or when other precipitating factors are superimposed. The onset of overt heart failure heralds a bleak outcome. These structural and functional changes associated with hypertension evolve over decades and are preventable with effective antihypertensive treatment. These observations emphasize the importance of early diagnosis and effective treatment of hypertension to prevent cardiac complications.

Heart Failure↗
PubMed1998

Evaluation of left ventricular diastolic function from the pattern of left ventricular filling.

The pattern of left ventricular (LV) filling can be determined by Doppler echocardiography. Normally most LV filling occurs early in diastole, with some additional filling occurring during atrial systole, late in diastole. In the absence of mitral stenosis, three patterns of LV filling indicate progressively greater diastolic dysfunction: (1) Reduced early diastolic filling with a compensatory increase in importance of atrial filling, termed a pattern of "impaired relaxation;" (2) "pseudo-normalization" with most filling early in diastole but with rapid deceleration of mitral flow; and (3) "restricted filling" with almost all filling of the LV occurring very early in diastole in association with very rapid deceleration of mitral flow. A large, prolonged atrial regurgitant flow in the pulmonary veins also indicates impaired diastolic performance. The time for early filling deceleration is predominantly determined by LV stiffness: the shorter the deceleration time, the stiffer the LV. Patients with short deceleration time have a poor prognosis.

Blood Flow Velocity↗
PubMed1987

Subclinical left ventricular abnormalities in young subjects with long-term type 1 diabetes mellitus detected by digitized M-mode echocardiography.

Noninvasive studies in patients with type 1 diabetes mellitus suggest subclinical left ventricular (LV) impairment, but the studies differ with regard to methods, patient selection and results. Thus, digitized M-mode echocardiograms were recorded in 24 persons younger than 50 years with long-term (more than 12 years) type 1 diabetes but without overt heart disease and in 28 control subjects. To improve accuracy, measurements were adjusted for body surface area, LV size and the influence of heart rate, as appropriate. Diabetics had a higher heart rate and systolic and diastolic blood pressure than control subjects. LV end-diastolic and stroke dimensions were smaller, duration of systole longer and preejection period/LV ejection time ratio higher than in control subjects, whereas fractional shortening and peak shortening rate were similar. In diabetics, diastole was shorter, peak filling rate was lower and the rapid filling period was prolonged, while percent filling during the rapid filling period and atrial contribution to filling were higher. Thus, in a well defined study population of relatively young persons with long-term type 1 diabetes, subclinical LV systolic and diastolic dysfunction were found. The diastolic abnormalities suggest reduced LV compliance, while those in systole may be secondary to an increased afterload or decreased myocardial contractility.

Adult↗
PubMed2000

Invasive and non-invasive determinants of pulmonary hypertension in patients with chronic heart failure.

BACKGROUND: In patients with chronic heart failure, pulmonary hypertension is an important predictive marker of adverse outcome. Its invasive and non-invasive determinants have not been evaluated. OBJECTIVE: This study was performed to evaluate hemodynamic determinants of pulmonary hypertension in chronic heart failure and to compare the predictive value of Doppler indices with that of invasively measured hemodynamic indices. METHODS: Right heart catheterization and transthoracic echo-Doppler were simultaneously performed in 259 consecutive patients with chronic heart failure (ejection fraction 24% +/- 7%) who were in sinus rhythm and receiving optimized medical therapy. Systolic pulmonary artery pressure (sPAP), cardiac index, transpulmonary gradient pressure, and pulmonary wedge pressure (PWP) were measured invasively. Left atrial and ventricular systolic and diastolic volumes, the ratio of maximal early to late diastolic filling velocities (E/A ratio), deceleration time (DT) and atrial filling fraction (AFF) of transmitral flow, systolic fraction of forward pulmonary venous flow (SFpvf), and mitral regurgitation were quantified by echo-Doppler. RESULTS: Patients with pulmonary hypertension had greater left atrial systolic and diastolic dysfunction, more left ventricular diastolic abnormalities, and greater hemodynamic impairment. The correlations between systolic left ventricular indices, mitral regurgitation, and sPAP were generally poor. Among invasive and non-invasive measurements, PWP (r = 0.89, p < 0.0001) and SFpvf (r = -0.68, p < 0.0001) showed the strongest correlation with sPAP. When we compared all patients with those without mitral regurgitation, the correlations between E/A ratio (r = 0.56 vs r = 0. 74, p < 0.002), SFpvf (r = -0.68 vs r = -0.84, p < 0.03), and systolic pulmonary artery pressure were significantly stronger. Multivariate analysis revealed that PWP was the strongest invasive independent predictor of systolic pulmonary artery pressure in patients with (R(2) = 0.87, p < 0.0001) and without (R(2) = 0.90, p < 0.0001) mitral regurgitation. A PWP > or= 18 mm Hg (odds ratio [95% CL], 142 (41-570) was strongly associated with systolic pulmonary hypertension. Among non-invasive variables DT, SFpvf, and AFF were identified as independent predictors of sPAP in patients with (R(2) = 0.56, p < 0.0001) and without (R(2) = 0.78, p < 0.0001) mitral regurgitation. A DT < 130 (odds ratio [95% CL], 3.5 (1.3-8.5), SFfvp < 40% (odds ratio [95% CL], 333 (41-1,007), and AFF < 30% (odds ratio [95% CL], 2 (1.3-7) most strongly predicted systolic pulmonary hypertension. CONCLUSIONS: The results of this study indicate that in patients with chronic heart failure, venous pulmonary congestion is an important determinant of systolic pulmonary artery hypertension. Hemodynamic and Doppler determinants showed similar predictive power in identifying systolic pulmonary artery hypertension.

Blood Flow Velocity↗
PubMed1994

Doppler echocardiographic evaluation of left ventricular diastolic function in acute hypothyroidism.

OBJECTIVE: Left ventricular diastolic dysfunction is an important cause of symptomatic heart failure. Previous studies suggest that thyroid dysfunction affects left ventricular diastolic function but the underlying mechanisms remain controversial. The study was undertaken to asses the influence of acute hypothyroidism on left ventricular diastolic function and to elucidate possible underlying mechanisms by means of Doppler echocardiography in a group of athyreotic patients, whose thyroid state depended only on external thyroid hormone supply and could therefore easily be controlled. PATIENTS: Eleven patients (5 men, 6 women, aged 20-55 years), who had had total thyroidectomy, were investigated during mild hyperthyroidism and during acute hypothyroidism. Additionally, 11 healthy control subjects aged 25-51 years were included in the study. DESIGN: M-mode echocardiography of the left ventricle and pulsed-wave Doppler echocardiography of the transmitral flow velocity pattern were carried out. RESULTS: Acute hypothyroidism produced a decrease of left ventricular end-diastolic diameter from 48 +/- 5 to 46 +/- 5 mm (mean +/- SD P < 0.05), of peak velocity of early diastolic filling from 0.52 +/- 0.10 to 0.42 +/- 0.05 m/s (P < 0.05), of peak velocity of late diastolic filling from 0.42 +/- 0.10 to 0.36 +/- 0.09 m/s (P < 0.05), and a decreased time-velocity integral of early diastolic filling (6.2 +/- 1.8 vs 5.1 +/- 0.7 cm, P < 0.05). The other M-mode and Doppler echocardiographic parameters did not differ between the hyperthyroid and the hypothyroid states. CONCLUSIONS: The observed changes of the trans-mitral flow velocity pattern during acute hypothyroidism can be attributed to a reduction of pre-load. There is no direct evidence that acute hypothyroidism affects the intrinsic diastolic properties of the left ventricle.

Acute Disease↗
PubMed2005

Coronary reserve in Takayasu's arteritis: transesophageal echocardiographic analysis.

BACKGROUND: The incidence of coronary arteries lesion in Takayasu's arteritis varies from 9% to 10% and is usually discovered at autopsy. Recent studies have demonstrated the value of echocardiography in noninvasive detection of significant coronary stenosis. AIM: The aim of our study was to evaluate coronary reserve in 15 patients with Takayasu's arteritis using contrast transesophageal echocardiography (Optison). METHODS: Transesophageal echocardiogram under basal conditions and in the hyperemic phase with dipyridamole challenge, myocardial perfusion studies and coronary angiography were performed on all patients. Seventy-three percent of them had histories of systemic hypertension, and the most frequent cardiovascular symptoms were shortness of breath (80%), headache (46%), angina (40%), and dizziness (33%). RESULTS: The transthoracic echocardiogram showed left ventricular systolic dysfunction in 6% and diastolic dysfunction in 53%. Aortic regurgitation was found in 67% of the patients, and 60% had mitral and/or tricuspid regurgitation. Coronary reserve was diminished in 3 patients with significant coronary lesions and in 2 patients with coronary dilation (33%). In the 3 patients with obstructive lesions and diminished coronary reserve, reversible perfusion defects were found with thallium-201 single-photon emission computed tomography. One patient with coronary dilation had normal perfusion, while the other demonstrated reversible and irreversible perfusion defects. One patient without coronary lesions and with normal coronary reserve had an irreversible fibrotic changes and the other reversible defects due to abnormal microcirculation. CONCLUSIONS: Transesophageal echocardiography is a feasible and promising technique for assessing coronary reserve in patients with Takayasu's arteritis.

Adolescent↗
PubMed2001

[Effects of the dual chamber electrocardiostimulation on the systolic and diastolic function of the myocardium].

An assessment of the indicators of the systolic and diastolic functions of the left ventricle was made in 52 patients against the background of electrostimulation with a dual chamber electro-cardiostimulator with different atrioventricular delays (185, 125 and 79 ms). Different variants of the reactions to electrostimulation with a shorter atrioventricular delay were detected: the positive dynamics of the diastolic indicators was registered in the hypertrophic type of the diastolic dysfunction, aggravation of the diastolic disorders--in the restrictive type.

Adult↗
PubMed1997

[How to choose and adequate antihypertensive drug depending on the type of the existing heart damage?].

The main goal of the treatment for hypertensive vascular disease is to reduce the morbidity and mortality that follow the disease. In the patient with heart disease, the choice of antihypertensive treatment will depend on several factors, all of which must be considered prior to it: type of cardiopathy and complications, pharmacokinetics of the drug-selected and its side effects, interactions with specific treatment for the main heart disease, positive or negative interactions with risk factors and, finally, its prognostic benefits. In the present study we briefly analyze this considerations in relation to different diseases such as ischemic heart disease, ventricular dysfunction (hypertrophy, systolic and diastolic dysfunction), heart rhythm disorders (sinus node dysfunction, supraventricular and ventricular ectopies), vascular pathology (cerebral and peripheral vasculopathy) and risk factors (diabetes, dyslipemia, obesity). Based on this considerations, several recommendations are done in order to choose the best antihypertensive drug in such cardiovascular diseases.

Antihypertensive Agents↗
PubMedDate not supplied

[Diastolic left ventricular dysfunction--significance for differential diagnosis and therapy of heart failure in the aged].

The discrimination of the pathogenesis of the clinical picture "heart failure" as caused by a dominant systolic or diastolic LV-dysfunction is of a special importance in the elderly patient because of the consequences for the choice of pharmacological therapy, resulting from the age-related physiological increase of stiffness of the myocardium. The pathophysiology of diastolic dysfunction is characterized by a prolonged relaxation period as well as by compromised passive filling properties, caused by myocardial and external determinants. Typical clinical signs of diastolic dysfunction are dyspnea or pulmonary edema. Cardiac disorders with a dominance of diastolic dysfunction are coronary and hypertensive heart disease as well as hypertrophic or uremic cardiomyopathies. Diagnosis of diastolic dysfunction easily can be performed noninvasively by means of Doppler-echocardiography. Pharmacological therapy in diastolic dysfunction should prefer beta blocking drugs and calcium-antagonists against vasodilators or digitalis.

Aged↗
PubMed2000

Doppler tissue imaging in congestive heart failure patients due to diastolic or systolic dysfunction: a comparison with Doppler echocardiography and the atrio-ventricular plane displacement technique.

BACKGROUND: Doppler tissue imaging (DTI) is an echocardiographic technique by which regional contractility, relaxation properties and time intervals are obtained easily. DTI has been reported to be relatively pre-load independent and could, in comparison with the commonly used mitral pulse wave Doppler (MPWD) method, be of clinical interest for identification of patients with diastolic dysfunction. The atrio-ventricular plane displacement (AVPD) method is an established technique to assess left ventricular systolic function. AIMS: To determine the pulsed Doppler DTI-pattern in patients with heart failure and to examine whether it has a similar capacity as MPWD and AVPD to diagnose diastolic dysfunction. METHODS: We studied 15 controls without congestive heart failure (CHF), 15 patients with diastolic (EF>45%+CHF) and 15 patients with systolic (EF<35%+CHF) left ventricular dysfunction and CHF. RESULTS: The DTI maximal velocities during systole (s), early filling wave (e) and atrial filling wave (a), decrease with reduced left ventricular ejection fraction, r=0.75, r=0.56 and r=0.66 (P<0.001) and regional isovolumetric contraction and intraventricular relaxation time measured by DTI are prolonged, r=0.59 and r=0.73, respectively (P<0.001). The 15 patients with diastolic heart failure were identified by MPWD or DTI but only 11 by AVPD with 8, 10 and 9 false-positive, respectively (P<0.01, P<0.05 and NS). CONCLUSIONS: Regional DTI show a consistent pattern in patients with left ventricular dysfunction and heart failure. Regional DTI has similar accuracy as MPWD in identifying diastolic heart failure patients and is superior to the AVPD technique. DTI may be a useful diagnostic tool in diastolic heart failure patients.

Aged↗
PubMed1997

Heart Failure in Elderly African-Americans.

Heart failure has emerged as one of the most important cardiovascular diseases in the elderly and has a major functional, economic, and social impact in older individuals. Racial differences in the morbidity and mortality, as well as in rates of hospitalization, have been reported in national surveys and epidemiologic studies. Because of the higher prevalence of hypertension and left ventricular hypertrophy in African-Americans compared to whites, these risk factors may be the principle determinants of the hemodynamic and clinical features of heart failure in African-Americans. The contribution of coronary disease with left ventricular remodeling secondary to myocardial ischemia or infarction varies among African-American populations, depending on the prevalence and impact of traditional risk factors for coronary heart disease. Atherosclerosis may play a greater role in the pathogenesis of heart failure in African-Americans as the impact of urbanization and the adoption of unhealthy lifestyles results in increased prevalence of risk factors for coronary artery disease. The hemodynamic and functional features of ventricular dysfunction in African-Americans with heart failure may range from asymptomatic diastolic dysfunction to typical systolic dysfunction. The differentiation of diastolic from systolic dysfunction, and hypertensive from ischemic cardiomyopathy, may be difficult in African-Americans and usually requires utilization of noninvasive cardiac diagnostic techniques. In addition to the type of ventricular dysfunction and the role of neurohormonal activation, consideration of age-related differences, ventricular structure and function, and variations in drug metabolism and pharmacokinetics are important.

Journal Article↗