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PubMed1988

Patterns of diastolic dysfunction in left ventricular hypertrophy.

The relative sensitivities of and interrelations between different measurements of diastolic function were studied in 50 patients with left ventricular hypertrophy diagnosed on anatomical grounds. Isovolumic relaxation time, the interval from minimum cavity dimension to mitral valve opening and relative dimension increase during this period, and the peak rate of dimension increase and wall thinning during rapid ventricular filling were measured by digitised M mode echocardiography. The relative heights of peak early diastolic and atrial velocities (a/E) and the time for decline of early diastolic velocity to half its peak value (velocity half time) were measured on continuous wave and pulsed Doppler and the relative height of the "a" wave was measured by apexcardiogram. All sets of values except those of the interval from minimum dimension to mitral opening were unimodally distributed, and all differed significantly from those in 20 age matched controls. The relative height of the "a" wave on the apexcardiogram (90% values were abnormal) was the most sensitive method of studying left ventricular diastolic function and peak rate of dimension increase was the least sensitive. Though none of the correlations was high, there were individual associations between peak rate of dimension increase, a/E, peak wall thinning rate, and velocity half time, and independently between delay in mitral valve opening and dimension change during this period. Other values seemed to be independent of one another, suggesting a different physiological basis. It is concluded that these various abnormal values do not reflect a single underlying disturbance of diastolic function. There are at least four possible discrete abnormalities: prolongation of isovolumic relaxation; incoordination during isovolumic relaxation; reduced rate of rapid filling; and an increase in the relative amplitude of the "a" wave probably caused by increased passive stiffness. These may be present singly or in combination in any patient.

Adolescent↗
PubMed1990

Left ventricular diastolic dysfunction in type 1 (insulin-dependent) diabetic patients during dynamic exercise.

The left ventricular diastolic and systolic functions were assessed in 27 strictly selected type 1 diabetic patients without overt heart disease and 50 age- and sex-matched control subjects. For evaluating left ventricular performance, complex mechanocardiography including digitized apexcardiography was used at rest and after symptom-limited, graded dynamic exercise. The values of diastolic/systolic time intervals and amplitude parameters did not differ significantly between the diabetic and control groups at rest. A longer value of corrected early apexcardiographic relaxation time (diabetics: 38.7 +/- 2.6 ms, controls: 17.3 +/- 2.1 ms, p less than 0.001) and a smaller normalized amplitude of relaxation (diabetics: 0.014 +/- 0.004 ms-1, controls: 0.056 +/- 0.006 ms-1, p less than 0.001) were observed after dynamic exercise suggesting disturbances of the early diastole in diabetic patients. No correlations could be found between the diastolic abnormalities and the diabetic control. Significant correlation was observed between the diastolic disorders and the duration of diabetes mellitus. Testing left ventricular performance by complex mechanocardiography including digitized apexcardiography after dynamic exercise in patients with type 1 diabetes might be useful for recognizing diastolic abnormalities even when no alterations could be identified at rest. Diastolic disorders could appear in diabetic patients without overt heart disease and clinical symptoms. Left ventricular systolic function might be normal, although exercise-induced alterations of diastolic function might already be present in type 1 diabetic patients.

Adolescent↗
PubMed1992

Left ventricular systolic and diastolic dysfunction after infusion of tumor necrosis factor-alpha in conscious dogs.

We used a load-insensitive index of systolic left ventricular (LV) function and an analysis of diastolic pressure-dimension relationships to test the hypothesis that recombinant human (rh) tumor necrosis factor-alpha (TNF alpha) impairs LV function in dogs. Animals were studied 7-10 d after aseptic implantation of instrumentation to monitor cardiac output, external anterior-posterior LV diameter, and LV and pleural pressures. Data were analyzed from seven dogs that received active rhTNF alpha (100 micrograms/kg over 60 min) and from five dogs that received heat-inactivated rhTNF alpha. At 24 h after infusion of active rhTNF alpha, the slope of the LV end-diastolic dimension-stroke work relationship decreased significantly, indicating a decrement in LV systolic contractility. Simultaneously, LV unstressed dimension increased significantly, suggesting diastolic myocardial creep. The end-diastolic relationship between LV transmural pressure and normalized LV dimension (strain) was markedly displaced to the left, suggesting increased diastolic elastic stiffness. Despite these changes in LV performance, cardiac index was maintained by tachycardia. The abnormalities in LV function were resolved by 72 h. We conclude that rhTNF alpha reversibly impairs LV systolic and diastolic function in unanesthetized dogs. Because dysfunction occurs greater than 6 h after the infusion of rhTNF alpha and persists for 24-48 h, the mechanism underlying this phenomenon may involve secondary mediators or a change in myocardial gene expression.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Diastolic dysfunction in patients with non-insulin-dependent diabetes mellitus of short duration.

To determine whether abnormal left ventricular diastolic function is present at an early stage of non-insulin-dependent diabetes mellitus (NIDDM), left ventricular diastolic filling was evaluated by pulsed doppler echocardiography in 16 normotensive patients with NIDDM of short duration (1.8 +/- 1 years, mean +/- SD) and no evidence of microangiopathy, and in 16 healthy volunteers comparable for age, body mass index, and sex distribution. All patients showed normal systolic function. The interventricular septum thickness, left atrial diameter, and left ventricular mass index were increased in the diabetic as compared with the control group (p < 0.01, p < 0.01, and p < 0.02, respectively). Isovolumic relaxation time and atrial peak filling velocity were greater in diabetic patients (p < 0.001, and p < 0.01, respectively), whereas early to atrial peak filling velocity ratio was significantly reduced (p < 0.05). This study demonstrates that an impairment of left ventricular diastolic function occurs early in the natural history of NIDDM, and that this abnormality is unlikely to be related to clinical evidence of microangiopathic complications.

Acute Disease↗
PubMed2001

Exercise training attenuates age-associated diastolic dysfunction in rats.

BACKGROUND: In contrast to systolic function, which is relatively well preserved with advancing age, diastolic function declines steadily after age 30. Our goal was to determine whether changes in diastolic function that occur with aging could be reversed with exercise training. Methods and Results-- Adult (6-month-old) and old (24-month-old) Fischer 344/BNF1 rats were studied after either 12 weeks of treadmill training or normal sedentary cage life. Three aspects of diastolic function were studied: (1) left ventricular (LV) filling in vivo via Doppler echocardiograph, (2) LV passive compliance, and (3) the degree of ischemia-induced LV stiffening. Maximal exercise capacity was lower in the old rats (18+/-1 minutes to exhaustion on a standard treadmill) than in the adult rats (25+/-1 minutes). Training increased exercise capacity by 43% in the old rats and 46% in the adults (to 26+/-1 and 37+/-1 minutes, respectively). Echocardiographic indices of LV relaxation were significantly lower in the old rats, but with training, they increased back to the levels seen in the adults. LV stiffness measured in the isolated, perfused hearts was not affected by age or training. Also in the isolated hearts, the LV stiffened more rapidly during low-flow ischemia in the old hearts than in the adults, but training eliminated this age-associated difference in the response to ischemia. CONCLUSIONS: Our findings indicate that in rats, some age-associated changes in diastolic function are reversible and thus may not be intrinsic to aging but instead secondary to other processes, such as deconditioning.

Aging↗
PubMed1996

Mechanisms and management of heart failure due to diastolic dysfunction.

A significant subset of patients with chronic heart failure have preserved systolic function and their symptoms are attributable to left ventricular diastolic abnormalities. In the setting of diastolic heart failure, the cardiac chambers are nondilated and have normal contractility, but left ventricular filling is impaired. This impairment in diastolic filling is related to both abnormalities of the passive elastic properties of the ventricle and impaired active relaxation as a result of any of the following: myocardial ischemia, hypertrophy, reduced beta-adrenergic tone, or increases in myocardial connective tissue. Therapy of diastolic heart failure is aimed at preventing and reducing left ventricular hypertrophy, treating elevated blood pressure, and reducing left ventricular filling pressure without reducing cardiac output. This may be achieved by maintaining sinus rhythm, slowing heart rate, and treating ischemia. Although calcium-channel blockers, beta-blockers, angiotensin-converting enzyme inhibitors, diuretics, and nitrates may improve symptoms in patients with diastolic heart failure, there are few data to indicate that these agents have an important effect on prognosis. Further studies of patients with diastolic heart failure are needed to assess its prevalence, clinical characteristics, prognosis, and response to therapy.

Aging↗
PubMed2001

Diastolic dysfunction precedes myocardial hypertrophy in the development of hypertension.

BACKGROUND: Left ventricular (LV) hypertrophy and impaired diastolic function may occur early in systemic hypertension, but longitudinal studies are missing. METHODS: We performed an echocardiographic follow-up study in young initially normotensive male offspring of hypertensive (OHyp) (n = 25) and normotensive (ONorm) (n = 17) parents. Blood pressure (BP), LV mass, and mitral inflow were determined at baseline and after 5 years. Pulmonary vein flow pattern assessment and septal myocardial Doppler imaging were additionally performed at follow-up. RESULTS: At follow-up, BP was not significantly different between the two groups (128 +/- 11/84 +/- 10 v 123 +/- 11/81 +/- 5 mm Hg, OHyp v ONorm) but five OHyp had developed mild hypertension. LV mass index remained unchanged and was not different between the two groups at follow-up (92 +/- 17 v 92 +/- 14 g/m2). Diastolic echocardiographic properties were similar at baseline, but, at follow-up, the following differences were found: mitral E deceleration time (209 +/- 32 v 185 +/- 36 msec, P < .05) and pulmonary vein reverse A wave duration (121 +/- 15 v 107 +/- 12 msec, P < .05) were prolonged in the OHyp as compared to the ONorm. Compared to the normotensive subjects, the five OHyp who developed hypertension had more pronounced alterations of LV diastolic function, that is, significantly higher mitral A (54 +/- 7 v 44 +/- 9 cm/sec, hypertensives v normotensives, P < .05), lower E/A ratio (1.31 +/- 0.14 v 1.82 +/- 0.48, P < .05), increased systolic-to-diastolic pulmonary vein flow ratio (1.11 +/- 0.3 v 0.81 +/- 0.16, P < .005), longer myocardial isovolumic relaxation time (57 +/- 7 v 46 +/- 12 msec, P < .05) as well as smaller myocardial E (10 +/- 1 v 13 +/- 2 cm/sec, P < .05) and E/A ratio (1.29 +/- 0.25 v 1.78 +/- 0.43, P < .05), despite similar LV mass (91 +/- 16 v 93 +/- 18 g/m2). CONCLUSIONS: Over a 5-year follow-up, initially lean, normotensive, young men with a moderate genetic risk for hypertension, developed Doppler echocardiographic alterations of LV diastolic function compared to matched offspring of normotensive parents. These alterations were more pronounced in the OHyp who developed mild hypertension and occurred without a distinct rise in LV mass.

Adult↗
PubMed1991

[The presence of diastolic dysfunction in hypertensive patients without left ventricular hypertrophy].

BACKGROUND: Hypertension is associated with abnormalities in the diastolic left ventricular function. The present study was performed to evaluate whether diastolic function is impaired independently from myocardial hypertrophy. METHODS: 41 patients with essential hypertension who had never received antihypertensive therapy were evaluated. All patients had normal systolic function. VE wave, or early diastolic filling wave, and VA, or late diastolic filling wave, were measured by Doppler echocardiography, and the VE/VA ratio was used as index of diastolic function. RESULTS: The VE/VA ratio was abnormally reduced in 23 patients, of which only 9 had left ventricular hypertrophy on echocardiographic criteria. The patients with a reduced ratio were older (p less than 0.01) than patients with a normal ratio. VE/VA ratio was not correlated with left ventricular mass, but it was correlated with age (r = 0.4186, p less than 0.01). CONCLUSIONS: Left ventricular diastolic function is impaired in hypertension independently from hypertrophy. The myocardial abnormalities associated with aging might be the major determinants of this functional impairment.

Adult↗
PubMed1991

[Biologist's view on diastolic dysfunction].

Modern biology provides satisfactory explanations for the abnormalities of the different phases of relaxation and diastole. Ventricular filling depends on three factors: active relaxation; the only factor is the concentration of ATP which has to re-increase. This requires elimination of the cytoplasmic calcium which activates ATP-ase by the Ca2+ ATPase of the sarcoplasmic reticulum and the Na+/Ca2+ pump. In hypertrophy, the concentration of the first and the activity of the second are decreased; passive wall compliance, which depends on the quantity and quality of parietal collagen. This factor is partially regulated in the myocardium by the concentration of aldosterone and angiotensin II; atrial contraction, which depends on the size of the atria and their isomyosine content. This changes in atrial overload to a slow form of myosine, one of the mechanisms of adaptation.

Calcium↗
PubMed2001

The importance of pulmonary venous flow measurement for evaluating left ventricular end-diastolic pressure in patients with coronary artery disease in the early stage of diastolic dysfunction.

Transmitral flow pattern assessed by pulsed Doppler echocardiography is widely used to evaluate left ventricular end-diastolic pressure (LVEDP). A restrictive mitral flow pattern is well recognized as a finding of severely elevated LVEDP. On the other hand, an abnormal relaxation pattern can be interpreted many ways. For example, some patients who display an abnormal relaxation pattern have a mild impairment of left ventricular (LV) relaxation as a result of aging, and others have severely impaired LV diastolic function. To evaluate LVEDP in patients with abnormal relaxation mitral filling patterns, we studied 55 patients who had coronary artery disease with abnormal relaxation pattern who underwent elective cardiac catheterization. We recorded the transmitral and pulmonary venous flow velocity curves and measured the duration of the mitral A wave (MAd) and pulmonary venous reversal wave during atrial contraction (PAd). Positive correlations were found between PAd and LVEDP (r = 0.65, P <.01) and between PAd-MAd and LVEDP (r = 0.7, P <.0001); however, MAd was not significantly correlated with LVEDP. In conclusion, PAd must be measured for an accurate evaluation of LV end-diastolic pressure in patients with an abnormal relaxation pattern in the transmitral flow velocity curve.

Aged↗
PubMed2002

Prognostic significance of left ventricular diastolic dysfunction in essential hypertension.

OBJECTIVES: We sought to assess the prognostic value of alterations in left ventricular (LV) diastolic function in patients with essential hypertension. BACKGROUND: Alterations in LV diastolic function are frequent in patients with hypertension, even in the absence of LV hypertrophy, but their prognostic significance has never been investigated. METHODS: In the setting of the Progetto Ipertensione Umbria Monitoraggio Ambulatoriale (PIUMA) study, we followed, for up to 11 years (mean: 4.4 years), 1,839 Caucasian hypertensive patients (50 +/- 12 years, 53% men, blood pressure (BP) 156/98 mm Hg) without previous cardiovascular events, who underwent Doppler echocardiography and 24-h BP monitoring before therapy. The early/atrial (E/A) mitral flow velocity ratio was calculated and corrected for age and heart rate (HR). RESULTS: During follow-up, there were 164 major cardiovascular events (2.04 per 100 patient-years). The incidence of cardiovascular events was 2.47 and 1.65 per 100 patient-years in patients with an age- and HR-adjusted E/A ratio below (n = 919) and above (n = 920) the median value, respectively (p < 0.005 by the log-rank test). In Cox analysis, controlling for age, gender, diabetes, cholesterol, smoking, LV mass and 24-h systolic BP (all p < 0.05), a low age- and HR-adjusted E/A ratio conferred an increased risk of cardiovascular events (odds ratio 1.57, 95% confidence interval [CI] 1.11 to 2.18, p < 0.01). A 21% excess risk was found for each 0.3 decrease of the adjusted E/A ratio (95% CI from +2% to +43%; p = 0.03). CONCLUSIONS: Impaired LV early diastolic relaxation, detected by pulsed Doppler echocardiography, identifies hypertensive patients at increased cardiovascular risk. Such association is independent of LV mass and ambulatory BP.

Adult↗