Ventricular Diastolic Dysfunction In Patients Research Articles

Left Ventricular Diastolic Dysfunction in Patients With Hypertension and Preserved Systolic Function

Left Ventricular Diastolic Dysfunction in Patients With Hypertension and Preserved Systolic Function

Left Ventricular Diastolic Dysfunction in Patients with Subclinical Hypothyroidism

Left Ventricular Diastolic Dysfunction in Patients with Subclinical Hypothyroidism

Use of Intraventricular Dispersion of the Peak Diastolic Flow Velocity as a Marker of Left Ventricular Diastolic Dysfunction in Patients with Atrial Fibrillation

The aim of this study was to evaluate the use of intraventricular dispersion of the peak diastolic flow velocity as a marker of left ventricular diastolic dysfunction in patients with atrial fibrillation. Regional diastolic flow velocity patterns at 1, 2, and 3 cm away from the mitral tip toward the apex were simultaneously recorded with the mitral flow velocity pattern by using pulsed Doppler echocardiography in 24 patients with atrial fibrillation before electrical or medical cardioversion. Echocardiographic examination was repeated after 10 to 30 days (ie, at the time of recovery of left atrial mechanical functions) after cardioversion of atrial fibrillation in all patients. Thirteen patients were found to have diastolic dysfunction; the remaining 11 patients with a normal E/A ratio constituted the control group. Afterward, the data recorded before the cardioversion were analyzed for each patient. In subjects with normal diastolic function, the peak diastolic flow velocity (PDFV) at the mitral tips also was maintained at the positions 1 to 3 cm away from the tip in the left ventricular cavity (PDFV at the mitral tips: 0.84 m/s, PDFV at 3 cm: 0.85 m/s; P = .34). In contrast, the regional PDFV progressively decreased toward the apex in patients with diastolic dysfunction (PDFV at the mitral tips: 0.82 m/s, PDFV at 3 cm: 0.63 m/s; P = .0004). Only 77% of the initial velocity was maintained at 3 cm away from the mitral tips in patients with diastolic dysfunction, whereas almost 100% of the initial velocity was preserved in patients with normal diastolic function ( P < .001). These findings suggest that the assessment of the intraventricular decrease in mitral PDFV may be used as a reliable marker of diastolic dysfunction in patients with atrial fibrillation. (J Am Soc Echocardiogr 1998;11:1036-43.)

Parasympathetic Neuropathy Associated with Left Ventricular Diastolic Dysfunction in Patients with Insulin-Dependent Diabetes Mellitus

Patients with insulin-dependent diabetes mellitus (IDDM) may develop autonomic neuropathy (AN) and cardiac complications. The association between AN and cardiac dysfunction was assessed in 34 IDDM patients (age 40 years, diabetes duration 21 years, 15 women) by echocardiography/Doppler and autonomic nerve function tests. The expiration/inspiration ratio (E/I) was used to assess parasympathetic damage, and the acceleration and brake indices for assessment of sympathetic impairment. AN was present in 21 patients. Patients with abnormal E/I (n = 11) had lower E/A ratios than patients without AN; early to atrial peak filling ratio (E/A) was median 1.1 (inter-quartile range 0.2) vs 1.4 (0.7), p = 0.022; early to atrial integral filling ratio (E/A) was 1.7 (0.3) vs 2.3 (1.2), p = 0.006. Patients with AN and normal E/I (sympathetic neuropathy, n = 10) and patients without AN had similar E/A ratios. E/A was also lower in patients with abnormal E/I compared with patients with AN and normal E/I; 1.7 (0.3) vs 2.2 (0.7), p = 0.008. Systolic function and cardiac dimensions were generally unaffected and similar in the three groups. In conclusion, diastolic dysfunction and parasympathetic neuropathy are related in IDDM patients.

Right and left ventricular diastolic dysfunction in patients with myocardial infarction: a color M-mode analysis

Right and left ventricular diastolic dysfunction in patients with myocardial infarction: a color M-mode analysis

Doppler Echocardiographic Detection of Left Ventricular Diastolic Dysfunction in Patients With Pulmonary Sarcoidosis

To determine the prevalence of left ventricular diastolic dysfunction in patients with biopsy specimen-proved pulmonary sarcoidosis without clinical evidence of cardiac disease. A cross-sectional study. A large tertiary care university teaching hospital. Fifty consecutive subjects had biopsy specimen-proved pulmonary sarcoidosis without suspected cardiac involvement. Those with other conditions known to affect diastolic function were excluded. The control group comprised 30 healthy hospital workers. Clinical examination, 12-lead ECG, and combined echocardiographic/phonocardiographic examination. Indexes of left ventricular diastolic function, including isovolumic relaxation time, peak velocity of early (E) and late (A) ventricular filling, deceleration rate of early diastolic flow, and the sum of the time velocity integrals of E and A were obtained in each patient and control subject. Systolic function was determined using a modification of Simpson's rule. Diastolic dysfunction was present in 7 (14%) patients, 6 of whom had normal systolic function and normal two-dimensional echocardiographic examination. Those with diastolic dysfunction had a longer duration of illness (15 +/- 7 vs 6 +/- 5 years; p = 0.0004), were significantly older (52 +/- 11 vs 38 +/- 9 years; p = 0.0009), and had higher systolic BP (130 +/- 13 vs 117 +/- 12 mm Hg; p = 0.01) than the sarcoid patients with normal diastolic function. These results demonstrate a significant prevalence of left ventricular diastolic dysfunction in patients with pulmonary sarcoidosis. The cause of this abnormality may be a subclinical sarcoid cardiomyopathy.

Left ventricular diastolic dysfunction as a cause of congestive heart failure. Mechanisms and management.

To define the mechanisms underlying left ventricular diastolic dysfunction in patients with congestive heart failure and normal systolic function and to identify the patients at risk for this syndrome. Studies were selected that describe the clinical observations of congestive heart failure with normal systolic function and that provide experimental and clinical insights into the mechanisms responsible for ventricular diastolic dysfunction. Recent studies indicate that a large number of patients (up to 40% in some series) presenting with congestive heart failure have preserved left ventricular systolic function. The factors contributing to altered left ventricular diastolic function include fibrosis, hypertrophy, ischemia, and increased afterload. The latter three factors, alone or in combination, predispose to impaired left ventricular relaxation, an active energy-requiring process. Thus, decreased left ventricular diastolic distensibility (increased diastolic pressure at any level of diastolic volume) may arise not only from altered passive elastic properties stemming from fibrosis or increased muscle mass but also from derangements in the dynamics of ventricular relaxation. In patients with essential hypertension, all four of the above mechanisms may be operative. Considering the prevalence of hypertension in the general population, hypertension appears to be an important underlying factor in many patients with heart failure on the basis of diastolic mechanisms. In the patient presenting with dyspnea and elevated filling pressures, but with a nondilated, normally contracting ventricle, treatment with standard heart failure medications (such as digitalis, diuretics, and vasodilators) is often ineffective and may be deleterious. Such patients may respond more favorably to beta-blockers and calcium-channel blockers. Diastolic dysfunction should be considered in the patient presenting with heart failure symptoms but with normal systolic function, particularly in hypertensive patients with left ventricular hypertrophy.

Prevalence of unsuspected mitral regurgitation and left ventricular diastolic dysfunction in patients with coronary artery disease and acute pulmonary edema associated with normal or depressed left ventricular systolic function

To define the prevalence and role of left ventricular (LV) systolic dysfunction, LV diastolic dysfunction and mitral regurgitation (MR) in patients with acute pulmonary edema, 40 patients with coronary artery disease and acute pulmonary edema were prospectively evaluated within 36 hours of presentation. LV ejection fraction and 3 parameters of LV diastolic function were measured with radionuclide ventriculography, whereas MR was assessed with Doppler echocardiography. LV ejection fraction was normal in 11 (27%) and depressed in 29 (73%) patients. Moderate or severe MR without LV diastolic dysfunction was common and equally prevalent in patients with and without LV systolic dysfunction (33 vs 38%; difference not significant). Diastolic dysfunction without MR was less frequent but equally prevalent in patients with and without systolic dysfunction (17 vs 27%; difference not significant). Two (18%) of 11 patients without and 12 (33%) of 36 patients with LV systolic dysfunction had both MR and LV diastolic dysfunction. Furthermore, MR was clinically silent and unsuspected in two-thirds of all patients with MR, regardless of a normal or depressed systolic function. These data show that there is a high prevalence of unrecognized moderate to severe MR in patients with acute pulmonary edema, regardless of the presence or absence of LV systolic dysfunction. Furthermore, the prevalence of LV diastolic dysfunction without MR is relatively low even in patients with normal LV systolic function and pulmonary edema. Thus, unrecognized MR may be an important contributor to the syndrome of acute pulmonary edema in patients with normal or depressed LV systolic function.

Echo-Doppler study of stress-induced left ventricular diastolic dysfunction in patients with congestive heart failure

Echo-Doppler study of stress-induced left ventricular diastolic dysfunction in patients with congestive heart failure