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PubMed1997

Diastolic dysfunction of the left ventricle. A review of the physiology, causes, diagnosis, treatment and implications.

Diastolic dysfunction of the left ventricle frequently occurs in people with left ventricular hypertrophy and coronary artery disease. It is a common cause of congestive heart failure, especially in the elderly. The mechanism of diastolic dysfunction, its causes, diagnosis and treatment, are reviewed. These are important factors to a Medical Director who must assess the results of non-invasive studies. Alerted by the possibility of diastolic dysfunction, the Medical Director can be more sensitive to other signs and symptoms that may represent early signs of congestive heart failure or ischemia.

Aged↗
PubMed2000

Effects of a single dose of oral estrogen on left ventricular diastolic function in hypertensive postmenopausal women with diastolic dysfunction.

OBJECTIVE: To evaluate the acute effects of a single dose of oral estrogen on left ventricular diastolic function in hypertensive postmenopausal women with diastolic dysfunction. DESIGN: Prospective, double-blind, placebo-controlled, clinical study. SETTING: Cardiology and postmenopausal outpatient clinics of a university hospital. PATIENT(S): Thirty postmenopausal women with hypertension (diastolic blood pressure of >90 mm Hg) and left ventricular diastolic dysfunction (mitral E/A ratio [the ratio of peak velocity of early mitral diastolic filling to late diastolic filling] of <1 and isovolumic relaxation time of >100 ms) were included in the study. Thirty normotensive postmenopausal women with normal left ventricular diastolic function served as the control group. INTERVENTION(S): Conjugated equine estrogen (0.625 mg) was given orally. Left ventricular diastolic function was assessed by Doppler echocardiography at baseline and 3 hours after the administration of estrogen. MAIN OUTCOME MEASURE(S): Left ventricular diastolic filling as assessed by Doppler echocardiography. RESULT(S): Estrogen had no effect on heart rate or blood pressure in either study group. The baseline E/A ratios were 0.72 +/- 0.26 and 1.22 +/- 0.30, and the isovolumic relaxation times were 122 +/- 18 ms and 89 +/-14 ms in the hypertensive and normotensive groups, respectively. Estrogen had no significant effect on any of the Doppler parameters in the normotensive group. In the hypertensive group, there was a trend toward normalization of the E/A ratio (from 0.73 +/- 0.11 to 0.84 +/- 20) and a significant improvement in the isovolumic relaxation time (from 124 +/- 20 ms to 105 +/- 13 ms) in response to the administration of estrogen compared with placebo. CONCLUSION(S): A single dose of oral estrogen caused a significant improvement in left ventricular diastolic filling in hypertensive postmenopausal women with diastolic dysfunction.

Blood Pressure↗
PubMed2000

Lack of direct role for calcium in ischemic diastolic dysfunction in isolated hearts.

BACKGROUND: Ischemia is characterized by an increase in intracellular calcium and occurrence of diastolic dysfunction. We investigated whether the myocyte calcium level is an important direct determinant of ischemic diastolic dysfunction. METHODS AND RESULTS: We exposed isolated, perfused isovolumic (balloon in left ventricle) rat and rabbit hearts to low-flow ischemia and increased extracellular calcium (from 1.5 to 16 mmol/L) for brief periods. Intracellular calcium was measured by aequorin. Low-flow ischemia resulted in a 270% increase (P:<0.05) in diastolic intracellular calcium, a 50% (P:<0.05) calcium transient amplitude decrease, and a 52% (P:<0.05) slowing of calcium transient decline. Diastolic pressure increased by 6+/-2 mm Hg (P:<0.05), and rate of systolic pressure decay decreased by 65% (P:<0.05). Experimentally increasing extracellular calcium doubled both intracellular diastolic calcium and calcium transient amplitude, concomitant with a developed pressure increase; however, there was no increase in ischemic diastolic pressure, slowing of the calcium transient decay, or further slowing of systolic pressure decay. Similarly, after 45 minutes of low-flow ischemia, after diastolic pressure had increased from 8.5+/-0.6 to 19.7+/-3.5 mm Hg (P:<0.001), intracoronary high-molar calcium chloride infusion increased systolic pressure from 36+/-4 to 63+/-11 mm Hg (P:<0.001), indicating an increase in intracellular calcium, but it decreased diastolic pressure from 19. 7+/-3.5 to 17.5+/-3.7 mm Hg (P:<0.01). Conversely, EGTA infusion decreased systolic pressure, indicating a decrease in intracellular calcium, but did not decrease diastolic pressure. CONCLUSIONS: When calcium availability was experimentally altered during ischemia, there was no alteration in left ventricular diastolic pressure, suggesting that ischemic diastolic dysfunction is not directly mediated by a calcium activated tension.

Animals↗
PubMed1993

Reversible left ventricular diastolic dysfunction resulting from frequent supraventricular tachycardia.

In two patients with frequent supraventricular tachycardia, echocardiograms revealed remarkable left ventricular systolic and diastolic dysfunction, associated with an absence of left ventricular filling during the early diastolic phase. This dysfunction was detected during normal sinus rhythm as well as tachycardia. By treatment with propafenone, both patients showed dramatic and rapid improvement of symptoms and the left ventricular dysfunction. Left ventricular diastolic dysfunction as well as systolic dysfunction were detected in patients with supraventricular tachycardia, suggesting that frequent supraventricular tachycardia results in severe left ventricular diastolic dysfunction which is reversible after control of the tachycardia.

Aged↗
PubMed1999

Congestive heart failure arising from diastolic dysfunction in the presence of normal left-ventricular systolic function.

Congestive heart failure due to diastolic dysfunction is a common clinical entity, particularly in the elderly. As outlined, such patients fall into a larger group of all patients with CHF symptoms and normal systolic function. When finding "normal" systolic function, the clinician should embark upon a carefully outlined diagnostic work-up geared toward eliminating confounding or treatable contributing causes of dyspnea or typical CHF symptoms. The prognosis for CHF patients with primarily diastolic dysfunction is not as poor as for those with LV systolic dysfunction, although the prevalence, associated morbidity, and costs are great. In contrast to the large number of successful clinical trials that have guided treatment of LV systolic failure, an extremely limited number of trials have specifically addressed themselves to diastolic dysfunction. Marked symptomatic relief can often be provided with careful attention to tailored therapy, although little is known with regard to outcome. Refinements in noninvasive imaging methods and hemodynamic indices of diastolic function may lead to improved patient care.

Diastole↗
PubMed1999

Heart failure: clinical implications of systolic and diastolic dysfunction.

Morbidity and mortality from congestive heart failure (CHF) remain high for older patients with systolic or diastolic dysfunction. These two disease processes differ in clinical manifestations, physical findings, treatment options, and prognosis. No one physical findings is diagnostic, which underlines the importance of assessing LV function with Doppler echocardiography. Diastolic dysfunction has been shown to increase with age, although most data demonstrating effective medical therapy for CHF applies to patients with systolic dysfunction. The treatment of older patients with preserved systolic function and CHF is therefore difficult, due to incomplete understanding of diastolic dysfunction and limited data about specific drug therapies.

Aged↗
PubMed1995

Diastolic dysfunction in patients on thyroid-stimulating hormone suppressive therapy with levothyroxine: beneficial effect of beta-blockade.

Thyroid-stimulating hormone (TSH) suppressive therapy with levothyroxine (L-T4) may cause adverse cardiac effects such as rhythm disturbances and ventricular hypertrophy. The latter is a predisposing condition to diastolic dysfunction. Thus, this study was designed to assess the effect of long-term TSH suppressive therapy on cardiac diastolic function. Because beta-blockade is known to reduce ventricular hypertrophy in patients on L-T4 therapy, we also tried to determine whether the addition of a beta-blocker to L-T4 improved diastolic function. Twenty-five patients (21 female and 4 male; mean age 41 +/- 10 yr) on TSH suppressive therapy for 3-9 yr (9 for differentiated carcinoma and 16 for nontoxic goiter) and 20 control subjects were studied. A subgroup of 10 patients, selected for the presence of symptoms and signs of adrenergic overactivity, was treated for 4 months with the beta-blocker bisoprolol (4.25 +/- 1.2 mg/day), and their maintaining L-T4 therapy was unchanged. In the patient group, left ventricular mass was significantly increased (P < 0.001), isovolumic relaxation time was prolonged (P < 0.001), and early diastolic filling velocity was markedly reduced (P < 0.001), whereas late diastolic filling was increased (P < 0.005). Consequently, the early-to-late diastolic flow velocity ratio was markedly decreased (P < 0.001). These alterations were more pronounced in the subgroup of patients with evidence of adrenergic overactivity. In these patients, beta-blockade induced a significant regression of cardiac hypertrophy and improved diastolic dysfunction. In particular, isovolumic relaxation time decreased (P < 0.01) and the early-to-late flow velocity ratio increased significantly (P < 0.01). Both indices reached values after beta-blockade that were no longer different from those of asymptomatic patients. It is concluded that long-term L-T4 therapy increases myocardial mass and causes relevant diastolic dysfunction, particularly in those patients with evidence of mild hyperthyroidism and adrenergic overactivity. Both myocardial hypertrophy and diastolic dysfunction are significantly improved by adrenergic beta-blockade.

Adult↗
PubMed1993

Isolated diastolic dysfunction of the myocardium and its response to CoQ10 treatment.

Symptoms of fatigue and activity impairment, atypical precordial pain, and cardiac arrhythmia frequently precede by years the development of congestive heart failure. Of 115 patients with these symptoms, 60 were diagnosed as having hypertensive cardiovascular disease, 27 mitral valve prolapse syndrome, and 28 chronic fatigue syndrome. These symptoms are common with diastolic dysfunction, and diastolic function is energy dependent. All patients had blood pressure, clinical status, coenzyme Q10 (CoQ10) blood levels and echocardiographic measurement of diastolic function, systolic function, and myocardial thickness recorded before and after CoQ10 replacement. At control, 63 patients were functional class III and 54 class II; all showed diastolic dysfunction; the mean CoQ10 blood level was 0.855 micrograms/ml; 65%, 15%, and 7% showed significant myocardial hypertrophy, and 87%, 30%, and 11% had elevated blood pressure readings in hypertensive disease, mitral valve prolapse and chronic fatigue syndrome respectively. Except for higher blood pressure levels and more myocardial thickening in the hypertensive patients, there was little difference between the three groups. CoQ10 administration resulted in improvement in all; reduction in high blood pressure in 80%, and improvement in diastolic function in all patients with follow-up echocardiograms to date; a reduction in myocardial thickness in 53% of hypertensives and 36% of the combined prolapse and fatigue syndrome groups; and a reduced fractional shortening in those high at control and an increase in those initially low.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

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

OBJECTIVE: 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. STUDY SELECTION: 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. DATA SYNTHESIS: 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. RESULTS: 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. CONCLUSIONS: 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.

Diastole↗
PubMed1998

Postoperative pulmonary edema secondary to diastolic dysfunction in a patient with a previous heart transplant.

Left ventricular diastolic dysfunction with preserved contractility is being recognized with increasing frequency. We describe a 53-year-old man who had undergone heart transplantation 10 years previously, who was now scheduled for renal biopsy for progressive and unexplained decline in renal function. Hypertension from pain or a stress response, increases in preload, and tachycardia predispose patients with chronic left ventricular diastolic dysfunction to pulmonary edema. Prompt and accurate diagnosis is essential for treatment. We recommend echocardiographic assessment of diastolic function when preoperative evaluation of left ventricular function is considered for these patients.

Biopsy↗
PubMed2001

Prevalence of diastolic dysfunction in normotensive, asymptomatic patients with well-controlled type 2 diabetes mellitus.

To evaluate the prevalence of left ventricular (LV) diastolic dysfunction in patients with type 2 diabetes mellitus free of cardiovascular disease, we studied 86 normotensive men and women (mean age 46 +/- 6 years) with Doppler echocardiography. All subjects were asymptomatic for ischemic heart disease or heart failure. The traditional transmitral filling patterns were used to characterize diastolic physiology. The Valsalva maneuver was used to differentiate normal from pseudonormal LV filling pattern. All patients had a normal electrocardiogram at rest and a negative result on exercise echocardiography for inducible wall motion abnormalities. Global LV systolic function was normal (mean LV ejection fraction 58%, range 53% to 76%). Diastolic dysfunction was found in 41 subjects (47%) of which 26 (30%) had impaired relaxation and 15 (17%) had a pseudonormal filling pattern. The mean LV mass index was 101 g/m2 (range 86 to 122). All patients with a normal-filling physiology had gender-adjusted normal LV mass index (mean 93 +/- 11 g/m2), whereas 62% of those with either abnormal relaxation (mean 103 +/- 12 g/m2, p <0.001) or a pseudonormal pattern (mean 110 +/- 12 g/m2, p <0.001) had increased LV mass index. No subject in this cohort had restrictive diastolic physiology. In conclusion, diastolic dysfunction in type 2 diabetes mellitus patients is often found despite adequate metabolic control and freedom from clinically detectable heart disease. The Valsalva maneuver can unmask an additional 17% of patients with subclinical abnormal LV filling pattern, who otherwise would be classified as having a normal diastolic physiology. Increased LV mass index is closely associated with abnormal LV filling characteristics.

Adult↗
PubMed1999

Losartan improves exercise tolerance in patients with diastolic dysfunction and a hypertensive response to exercise.

OBJECTIVES: The aim of the study was to test the hypothesis that angiotensin II (Ang II) blockade would improve exercise tolerance in patients with diastolic dysfunction and a marked increase in systolic blood pressure (SBP) during exercise. BACKGROUND: Diastolic dysfunction may be exacerbated during exercise, especially if there is a marked increase in SBP. Angiotensin II may contribute to the hypertensive response to exercise and impair diastolic performance. METHODS: We performed a randomized, double-blind, placebo-controlled, crossover study of two weeks of losartan (50 mg q.d.) on exercise tolerance and quality of life. The subjects were 20 patients, mean age 64 +/- 10 years with normal left ventricular systolic function (EF >50%), no ischemia on stress echocardiogram, mitral flow velocity E/A <1, normal resting SBP (<150 mm Hg), and a hypertensive response to exercise (SBP >200 mm Hg). Exercise echocardiograms (Modified Bruce Protocol) and the Minnesota Living With Heart Failure questionnaire were administered at baseline, and after each two-week treatment period, separated by a two-week washout period. RESULTS: Resting blood pressure (BP) was unaltered by placebo or losartan. During control, patients were able to exercise for 11.3 +/- 2.5 (mean +/- SD) min, with a peak exercise SBP of 226 +/- 24 mm Hg. After two weeks of losartan, baseline BP was unaltered, but peak SBP during exercise decreased to 193 +/- 27 mm Hg (p < 0.05 vs. baseline and placebo), and exercise time increased to 12.3 +/- 2.6 min (p < 0.05 vs. baseline and placebo). With placebo, there was no improvement in exercise duration (11.0 +/- 2.0 min) or peak exercise SBP (217 +/- 26 mm Hg). Quality of life improved with losartan (18 +/- 22, p < 0.05) compared to placebo (22 +/- 26). CONCLUSIONS: In patients with Doppler evidence of diastolic dysfunction at rest and a hypertensive response to exercise, Ang II receptor blockade blunts the hypertensive response to exercise, increases exercise tolerance and improves quality of life.

Adult↗
PubMed1999

Role of transesophageal echocardiography in assessing diastolic dysfunction in a large clinical practice: a 9-year experience.

BACKGROUND: Two-dimensional transthoracic echocardiography with respiratory monitoring has been used to characterize diseases that impair diastolic function. Transesophageal echocardiography (TEE) has emerged as a complementary technique to evaluate patients with these diseases. The purpose of this study was to evaluate in a large clinical practice the utility of TEE with respiratory monitoring for classification of patients with diastolic dysfunction. METHODS: Over a 9-year period TEE was used to examine 192 patients referred to an echocardiography laboratory for additional evaluation of abnormal diastolic function. We performed pulsed-wave Doppler TEE of the left ventricular inflow and pulmonary veins and respiratory monitoring to categorize patients as showing restrictive physiologic features, constriction with or without effusion, mixed constriction and restriction, abnormal relaxation, pseudonormalization, large pericardial effusion or tamponade, or normal diastolic function. RESULTS: Patients with diastolic dysfunction underwent 3% of the total number of transesophageal studies conducted during the study period. Among the 192 patients referred for TEE, abnormal diastolic function was found in 181 (94%); 11 (6%) had normal diastolic function. Seventy-one (39%) of the 181 patients had restrictive physiologic features. Constrictive pericarditis was found in 54 (30%) of the patients and was confirmed for all 31 patients who underwent pericardiectomy. Mixed constriction and restriction was present in 21 (12%) of the patients. The other 35 patients (19%) had abnormal relaxation, pseudonormalization, or large pericardial effusion or tamponade. The cause of diastolic dysfunction was idiopathic for 32% of the patients, previous cardiac operation for 26%, cardiac amyloidosis for 23%, radiation therapy for 11%, and hypertension or advanced ischemic heart disease for 8%. CONCLUSION: Two-dimensional and Doppler TEE with respiratory monitoring is useful in categorizing patients with impaired diastolic function, primarily into those with restrictive physiologic features or constrictive pericarditis.

Adult↗
PubMed1992

Exacerbation of left ventricular ischemic diastolic dysfunction by pressure-overload hypertrophy. Modification by specific inhibition of cardiac angiotensin converting enzyme.

Hearts with compensatory pressure-overload hypertrophy show an increased intracardiac activation of angiotensin II that may contribute to ischemic diastolic dysfunction. We studied whether pressure-overload hypertrophy in response to aortic banding would result in exaggerated diastolic dysfunction during low-flow ischemia and whether the specific inhibition of the cardiac angiotensin converting enzyme by enalaprilat would modify systolic and diastolic function during ischemia and reperfusion in either hypertrophied or nonhypertrophied hearts. Isolated, red blood cell-perfused isovolumic nonhypertrophied and hypertrophied rat hearts were subjected to enalaprilat (2.5 x 10(-7) M final concentration) infusion during 20 minutes of baseline perfusion and during 30 minutes of low-flow ischemia and 30 minutes of reperfusion. Coronary flow per gram was similar in nonhypertrophied and hypertrophied hearts during baseline perfusion, ischemia, and reperfusion. At baseline, left ventricular developed pressure was higher in hypertrophied than nonhypertrophied hearts in untreated groups (224 +/- 8 versus 150 +/- 9 mm Hg; p less than 0.01) and in enalaprilat-treated groups (223 +/- 9 versus 145 +/- 8 mm Hg; p less than 0.01). During low-flow ischemia, left ventricular developed pressure was depressed but similar in all groups. All groups showed deterioration of diastolic function; however, left ventricular end-diastolic pressure increased to a significantly higher level in untreated hypertrophied than in nonhypertrophied hearts (65 +/- 7 versus 33 +/- 3 mm Hg; p less than 0.001). Enalaprilat had no effect in nonhypertrophied hearts, but it significantly attenuated the greater increase in left ventricular end-diastolic pressure in hypertrophied hearts treated with enalaprilat compared with no drug (65 +/- 7 versus 50 +/- 5 mm Hg; p less than 0.01). The beneficial effect could not be explained by differences in coronary blood flow per gram left ventricular weight, glycolytic flux as reported by lactate production, myocardial water content, oxygen consumption, and tissue levels of glycogen and high energy phosphate compounds. During reperfusion, all hearts showed a partial recovery of developed pressure to 70-74% of initial values. No effect of enalaprilat could be detected during reperfusion on systolic and diastolic function or restoration of tissue levels of high energy compounds. In conclusion, our experiments show that hypertrophied red blood cell-perfused hearts manifest a severe impairment of left ventricular diastolic relaxation in response to low-flow ischemia in comparison with control hearts. Further, our experiments support the hypothesis that the enhanced conversion of angiotensin I to angiotensin II in rats with pressure-overload hypertrophy contributes to the enhanced sensitivity of hypertrophied hearts to diastolic dysfunction during low-flow ischemia.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Reversal of left ventricular diastolic dysfunction after kidney-pancreas transplantation in type 1 diabetic uremic patients.

OBJECTIVE: Diastolic function is frequently impaired in diabetic patients. Our aim was to evaluate the effects of glycometabolic control achieved by pancreas transplantation on left ventricular function in uremic type 1 diabetic patients. RESEARCH DESIGN AND METHODS: Left ventricular systolic and diastolic functions were evaluated using radionuclide ventriculography in 42 kidney-pancreas transplant patients and 26 kidney-alone recipients who had similar clinical characteristics before transplantation. Patients were grouped according to 6, 24, and 48 months of follow-up. Control subjects consisted of 20 type 1 diabetic patients. RESULTS: The left ventricular ejection fraction was normal in all of the patients. However, kidney-pancreas transplant patients with 4 years of graft function had a higher ejection fraction (75.7 +/- 1.8%) than kidney-alone patients with 4 years of graft function (65.3 +/- 2.8%, P = 0.02) and type 1 diabetic patients (61.3 +/- 3.7%, P = 0.004). In patients with 4 years of graft function, normal diastolic parameters were evident in kidney-pancreas but not in kidney-alone or in type 1 diabetic patients (peak filling rate: 4.46 +/- 0.15 end diastolic volume (EDV)/s in kidney-pancreas patients vs. 2.73 +/- 0.24 EDV/s [P < 0.01] and 3.39 +/- 0.30 EDV/s [P < 0.01] in kidney-alone and type 1 diabetic patients, respectively; time-to-peak filling rate: 141.9 +/- 7.8 ms in kidney-alone patients vs. 209.4 +/- 13.5 ms in kidney-alone patients [P < 0.01]; peak filling rate/peak ejection rate ratio: 1.10 +/- 0.04 in kidney-pancreas patients vs. 0.81 +/- 0.08 in kidney-alone patients [P < 0.01]). A significant reduction in diastolic dysfunction rate was observed only in kidney-pancreas patients. CONCLUSIONS: Kidney-pancreas transplantation results in complete insulin independence, a better glycometabolic pattern and blood pressure control, an improvement of left ventricular function, and a reversal of diastolic dysfunction.

Adult↗
PubMed1986

Alpha-adrenergic mechanisms in the pathophysiology of left ventricular heart failure--an analysis of their role in systolic and diastolic dysfunction.

Alpha-adrenoceptor (alpha-AR) mechanisms may contribute to systolic and diastolic dysfunction of the left ventricle. Centrally acting alpha 2-AR agonist drugs, including methyldopa, clonidine, and guanabenz, activate brainstem alpha 2-AR and this activation results in a decrease in overall sympathetic tone and an increase in parasympathetic tone. Peripherally acting alpha 1-AR antagonists, such as prazosin, inhibit the actions of catecholamines at post-synaptic receptor sites. Heart failure is characterized by hyperactivity of sympathetic pathways and parasympathetic withdrawal. In this situation, alpha 2-agonists reduce sympathetic activity and improve hemodynamic parameters of cardiac function; both acute and chronic administration of alpha 2-AR have been demonstrated to reduce serum catecholamine levels, heart rate, and arterial blood pressure, and to improve exercise performance. Diastolic dysfunction of the left ventricle is characterized by a marked decrease in ventricular compliance, often a result of hypertension and left ventricular hypertrophy; the end result is an increase in left ventricular filling pressure and pulmonary venous pressure. Treatment with alpha 2-AR, by decreasing sympathetic tone and blood pressure, and alpha 1-AR antagonists, by reducing blood pressure and by directly inhibiting the actions of catecholamines at alpha 1-AR, may produce a reduction in the degree of ventricular hypertrophy and improve diastolic performance of the left ventricle. Thus, therapeutic intervention in heart failure with either alpha 2-AR agonists or alpha 1-AR antagonists may favorably modulate these alterations in sympathetic tone and improve ventricular function.

Adrenergic alpha-Antagonists↗
PubMed1988

Effects of increasing afterload on early diastolic dysfunction in hypertrophic non-obstructive cardiomyopathy.

The effects of increasing afterload on early diastolic dysfunction in 10 patients with hypertrophic non-obstructive cardiomyopathy were studied by computer assisted analyses of digitised M mode echocardiograms. Infusion of angiotensin II increased the end systolic pressure by a mean (SD) of 36.2 (10.3) mm Hg. As the afterload increased early diastolic dysfunction tended to become more normal: the interval and the change in dimension between minimal cavity dimension and mitral valve opening decreased and the duration of rapid diastolic filling and the accompanying change in dimension increased. None the less, the end diastolic dimension and thus the overall diastolic filling remained unchanged. Impaired early diastolic function in hypertrophic cardiomyopathy is at least partly caused by altered loading conditions.

Adult↗
PubMed1996

Echocardiographic assessment of left ventricular hypertrophy diastolic dysfunction and pericardial disease in patients on maintenance haemodialysis.

Echocardiographic study of sixty patients on maintenance haemodialysis (MHD) was undertaken to determine the prevalence and factors associated with left ventricular (LV) hypertrophy (LVH), LV diastolic dysfunction and pericardial disease. The mean age was 34.4 (standard deviation 13.0), range 14-66 years with 31 (51.7%) men. LVH was found in 41 (68%) patients. Of the factors analysed, serum calcium and calcium-phosphate product were significantly associated with LVH (t = 2.01, df = 58, p = 0.046; t = 2.18, df = 58, p = 0.032 respectively). Hypertension in this study was not significantly associated with LVH (p = 0.169). LV diastolic dysfunction was found in 23/41 (56%) patients with LVH, and in 9/19 (47%) patients without LVH (difference is not statistically significant, X2 = 0.12, df = 1, p = 0.725). Small pericardial effusions were detected in 4/60 (7%) patients and two patients had pericardial thickening. We conclude that in our MHD patients LVH, is very common and that diastolic dysfunction is observed equally in patients with and without LVH. However, haemodynamically significant pericardial effusions are rare in patients who have been on dialysis for at least six months.

Adolescent↗