Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Diastolic Dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMedDate not supplied

The association between left ventricle diastolic dysfunction and endothelial dysfunction and the results of stress myocardial SPECT in asymptomatic patients with type 2 diabetes.

Diabetes mellitus is associated with a poor cardiovascular prognosis. Stress myocardial single-photon emission computed tomography (SPECT) reliably detects coronary ischaemia in asymptomatic patients. Our study aimed to evaluate the association between systolic and diastolic left ventricular function, left ventricular hypertrophy, endothelial function and the results of stress myocardial SPECT in 126 patients with type 2 diabetic patients with no cardiovascular symptoms. Thirty-three patients (26%) had abnormal SPECT results, 33 patients (26%) had intermediate (equivocal) results, and 60 patients (48%) had normal results. We found a significant association between an abnormal SPECT result, left ventricular diastolic dysfunction and impaired post-ischaemic dilatation of the brachial artery. No association was found between the SPECT result and systolic function and left ventricular hypertrophy, however. An abnormal SPECT result was significantly associated with left ventricular diastolic dysfunction and the deterioration of post-ischaemic dilatation of the brachial artery in asymptomatic patients with type 2 diabetes.

Aged↗
PubMed1991

Left ventricular diastolic dysfunction in patients with congestive heart failure.

This study reviewed 372 male patients with congestive heart failure. Two hundred and eighty-three (77%) had congestive heart failure due to systolic dysfunction as demonstrated by radionuclide angiography. Eighty-seven (23%) with congestive heart failure were identified who had normal ejection fractions. All patients met the Framingham criteria for congestive heart failure. These 87 individuals had unrecognized diastolic heart failure. It is important to distinguish between systolic and diastolic heart failure because the pathophysiology, treatment, and prognosis differ significantly. The most frequent cause of diastolic heart failure in this study was hypertension. Diastolic dysfunction should be considered in patients with acute heart failure and severe uncontrolled hypertension, or in patients with ischemic heart disease who develop acute pulmonary edema. Patients who do not respond or deteriorate when treated for heart failure using conventional therapy may also have diastolic dysfunction. These patients warrant special recognition and tailored management.

Aged↗
PubMed2002

Tei-Index in coronary artery disease--validation in patients with overall cardiac and isolated diastolic dysfunction.

BACKGROUND: The index "isovolumic contraction time and isovolumic relaxation time divided by ejection time" ("Tei-Index") has been demonstrated to provide useful information about disease severity and prognosis in patients with dilated cardiomyopathy and cardiac amyloidosis. In patients with coronary artery disease (CAD), the diagnostic utility of this index is unclear. We attempted to validate the Tei-Index in CAD patients with overall cardiac or isolated diastolic dysfunction. METHODS AND RESULTS: Sixty subjects were included who underwent left heart catheterization for invasive measurement of left ventricular end-diastolic pressure (LVEDP): 20 symptomatic CAD patients with overall cardiac dysfunction (defined by a LV ejection fraction (EF) < 45% (mean 27 +/- 8%) and a LVEDP > or = 16 mmHg, (mean 22 +/- 6 mmHg), NYHA class 2.7 +/- 0.4, OCD group), 29 symptomatic CAD patients with isolated diastolic dysfunction (defined by an EF > 45% (mean 55 +/- 8%), a normal end-diastolic diameter index (mean 2.8 +/- 0.4 cm/m2) and a LVEDP > or = 16 mmHg (mean 22 +/- 6 mmHg), NYHA class 2.3 +/- 0.4, IDD group) and 11 asymptomatic control subjects (EF 65 +/- 9%, LVEDP 11 +/- 4 mmHg, CON group). After conventional 2-D- and Doppler echocardiographic examination, the Tei-Index was obtained. The Tei-Index was easily and reproducibly measured in all study subjects. In the OCD group, isovolumic contraction time was prolonged and ejection time was shortened in comparison to the CON group, resulting in a significantly increased Tei-Index (0.71 +/- 0.28 vs 0.40 +/- 0.11, p < 0.01). In the IDD group, isovolumic relaxation time was prolonged and isovolumic contraction time was shortened in comparison to controls, resulting in a largely unchanged Tei-Index (0.45 +/- 0.14, p = ns). Receiver operating characteristic curve analysis for the Tei-Index yielded an area under the curve of 0.92 +/- 0.04 for separating patients with vs without OCD. Using a Tei-Index > 0.49 as a cut-off, OCD patients were identified with a sensitivity of 96% and a specificity of 86%. CONCLUSION: The Tei-Index is a valid and readily derived indicator of global cardiac dysfunction in CAD patients with impaired systolic and diastolic LV performance. The use of this index seems to be limited in CAD patients with primary diastolic dysfunction.

Aged↗
PubMed2006

[Glycosylated hemoglobin and left ventricular diastolic dysfunction in patients with type 2 diabetes mellitus].

UNLABELLED: Glycosylated hemoglobin (HbA1c) is a confirmed prognostic factor of cardiovascular complications in diabetic patients. The relative odds of cardiovascular disease (CD) increase by 20% for 1% increase of HbA1c above HbA1c 5%. The aim of the study was to assess relationship between diastolic dysfunction and HbA1c in patients with diabetes mellitus 2 (DM 2) without critical coronary stenosis in coronarography. MATERIAL AND METHODS: The study comprised 57 subjects (35 men and 22 women) with DM 2, without coronary stenosis in coronarography, with normal and elevated HbA1c levels. The subjects were divided into two groups depending on HbA1c level: with HbA1c < or = 6.1% and HbA1c >6.1%. Parameters of left ventricular diastolic function were assessed in echocardiography according to criterions of European Society of Cardiology. Subjects with decreased systolic function (EF<50%) were excluded from the study. RESULTS: Diastolic dysfunction of the left ventricle was observed in 43% of patients with HbA1c >6.1% comparing to 4.5% of patients in the group with HbA1 < or = 6.1%. In the group with HbA1c >6.1% in 38% of the patients abnormal relaxation in early filling phase and in 5% abnormal isovolumetric relaxation were observed. In the group with HbA1 < or = 6.1% in only 1 patient (4.5%) abnormal relaxation in early filling phase was observed. CONCLUSION: Diastolic function of the left ventricle in patients with diabetes is dependent on HbA1c levels.

Aged↗
PubMedDate not supplied

Myofibril MgATPase activities and energy metabolism in cardiomyopathic mice with diastolic dysfunction.

To study the genomic physiology of cardiac myofibril proteins in the heart, we have successfully created a cardiac troponin I (cTnI; a myofibril protein) gene knockout mouse model using gene targeting techniques. The phenotype of the cTnI gene knockout mouse is a cardiomyopathy with diastolic dysfunction resulting in sudden death in neonates. In the present studies, energy metabolism was analyzed in myocardial cells from cTnI-null hearts. Myofibril MgATPase activities were determined in myocardial cells from either wild-type or cTnI mutant mouse hearts. Furthermore, the quantity and quality of the mitochondria in wild-type and cTnI mutant animals were counted and analyzed. Our results demonstrate that damaged relaxation and increased Ca(2+)-independent force production in cTnI-null hearts is in part related to the increased myofibril MgATPase activities accompanied by an increase in mitochondria quantity and mitochondrial ATPase activities. These data indicate that cardiomyopathies with diastolic dysfunction are different from cardiomyopathies caused by systolic dysfunction. The former involves the damage of cardiac relaxation due to increased MgATPase activities and increased Ca(2+)-independent force production inside of myofilaments, while the latter involves the damage of systolic contraction due to decreased MgATPase activities and decreased force production.

Animals↗
PubMed2001

Maturation-dependent differences in regulation of sarcoplasmic reticulum Ca(2+) ATPase in sheep myocardium in response to pressure overload: a possible mechanism for maturation-dependent systolic and diastolic dysfunction.

We have previously demonstrated that pressure-overload hypertrophy in adult sheep is associated with myocardial dysfunction whereas that in young lambs is associated with normal contractility. To probe for possible mechanisms of these age-dependent differences, we assessed mRNA expression of genes encoding critical components of myocardial Ca(2+) handling in the same animal model. We studied left ventricular myocardium of young and adult sheep with short-term (48 h) and long-term (6 wk) pressure overload induced by ascending aortic constriction. Six weeks of pressure overload induced the significant left ventricular hypertrophy (36 and 39% increase in left ventricular/body weight ratio in lambs and sheep, respectively). The Ca(2+) ATPase and Na(+)/Ca(2+) exchanger mRNA decreased with pressure overload only in the adult (p < 0.05). Ca(2+) channel mRNA was slightly increased by pressure overload regardless of age (p < 0.05). Calsequestrin, sarcoplasmic reticulum Ca(2+) release channel, or myosin heavy-chain mRNA levels did not significantly differ. In adult sheep after 6 wk of pressure overload, decreases in load-adjusted midwall shortening (systolic dysfunction) and prolongation of relaxation time constant (diastolic dysfunction) correlated with decreases in Ca(2+)-ATPase mRNA. The sarcoplasmic reticulum Ca(2+)-ATPase protein level and Ca(2+) uptake activity of isolated sarcoplasmic reticulum vesicles were depressed only in the adult with pressure-overload hypertrophy but not in the young. We demonstrated age-dependent differences in mRNA expression of Ca(2+)-handling protein genes in response to pressure overload, which preceded the occurrence of hypertrophy and myocardial dysfunction. Thus, altered expression of Ca(2+)-handling protein genes may be one of the primary responses to pressure overload rather than a phenomenon secondary to myocardial hypertrophy.

Animals↗
PubMed1995

Diastolic dysfunction is a feature of the antiphospholipid syndrome.

Recurrent thrombi, thrombocytopenia, pregnancy loss, and stroke in association with medium to high concentrations of anticardiolipin antibodies are well-recognized features of antiphospholipid syndrome. Cardiac manifestations of primary antiphospholipid syndrome (PAPS) also have been documented but involve structural and valvular heart disease. Diastolic dysfunction in PAPS has not been well described. Therefore, 10 patients with PAPS (nine women and one man) of mean age 30 +/- 7 years (range 20 to 46 years) and 10 healthy age-, sex-, weight-, and height-matched control subjects were studied by echocardiography. Anticardiolipin antibody concentrations of patients with PAPS were > 80 immunoglobulin G phospholipid units as determined by enzyme-linked immunosorbent assay. Doppler-derived parameters of left ventricular filling showed a significant association between PAPS and diastolic dysfunction compared with control, as evidenced by a decrease in peak early filling velocity (52 +/- 10 cm/sec vs 67 +/- 12 cm/sec; p < 0.01), a decrease in the ratio of peak early to peak atrial filling velocities (1.03 +/- 0.40 vs 1.52 +/- 0.28; p < 0.005), a decrease in the mean deceleration rate of early filling (338 +/- 75 cm/sec2 vs 590 +/- 227 cm/sec2; p < 0.005), and an increase in the percentage of atrial contribution to filling and deceleration time. Left ventricular mass, diastolic filling time, and heart rate did not differ between groups. Left ventricular systolic function was normal and ejection fraction did not differ between patients with PAPS and control subjects (63% +/- 2% vs 65% +/- 7%; p not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Coronary flow reserve correlates left ventricular diastolic dysfunction in patients with dilated cardiomyopathy.

The relationship between altered coronary circulation and left ventricular (LV) function in dilated cardiomyopathy (DCM) remains unclear. We used the Doppler guidewire and transthoracic echo Doppler in 24 DCM patients to investigate the relationship between coronary flow reserve (CFR) and LV systolic/diastolic function, trying to predict diastolic dysfunction and evaluate DCM severity with CFR. CFR correlated better with the deceleration time (DT) of the E-wave and the ratio of E-wave peak value to that of the A-wave (E/A) than with LV ejection fraction (EF). The optimal CFR cutoff value for predicting the restrictive pattern of transmitral flow velocity (DT = 120 msec) was 2.6 (sensitivity 91%, specificity 100%). Dividing patients into two groups around the CFR = 2.6 cutoff, differences in DT and E/A between groups were more prominent than those for EF. CFR correlates better with LV diastolic than systolic function and may be useful for predicting diastolic dysfunction in DCM patients.

Adult↗
PubMed2005

Time-course of diastolic dysfunction in different stages of chronic HCV related liver diseases.

AIM: A hyperdynamic circulatory pattern in advanced liver disease is known since a long time. The first studies evaluating cardiac function in cirrhosis were performed in patients with alcoholic liver disease and thus this condition was attributed to the toxic effects of ethanol. A reduced performance of the left ventricle after physical and pharmacological strains along with an altered diastolic function has been demonstrated also in postviral cirrhosis. Many factors are involved in advanced cirrhosis whereas little is known in the earlier stages of disease. METHODS: To this aim we have investigated patients with different stages of hepatitis C virus (HCV)-related liver disease to detect the time-course of diastolic dysfunction. An impaired relaxation and increased thickness of left ventricular walls along with an altered pattern of transmitral flow can be easily detected by means of echocardiography. RESULTS: In chronic hepatitis diastolic function is preserved but increased thickness of left ventricle parietal walls can be detected in patients with fibrosis on liver biopsy. The typical pattern of diastolic dysfunction is observed in Child A cirrhotic patients and in Child C ascitic patients but thickness of parietal walls is more relevant in the former group. Chronic aldosterone blockade could exert favourable effects in heart remodeling suggesting a potential role of these drugs in cirrhotic cardiomyopathy. CONCLUSIONS: The presence of increased thickness of left ventricle parietal walls in chronic hepatitis C in the precirrhotic stage point to a putative role of HCV in this heart structural abnormality that can become a co-factor in the more advanced stages of cirrhosis when portal hypertension and its deleterious effects on systemic hemodynamics, cardiac function and structure become manifest.

Aged↗
PubMed1997

Postresuscitation left ventricular systolic and diastolic dysfunction. Treatment with dobutamine.

BACKGROUND: Global left ventricular dysfunction after successful resuscitation is well documented and appears to be a major contributing factor in limiting long-term survival after initial recovery from out-of-hospital sudden cardiac death. Treatment of such postresuscitation myocardial dysfunction has not been examined previously. METHODS AND RESULTS: Systolic and diastolic parameters of left ventricular function were measured in 27 swine before and after successful resuscitation from prolonged ventricular fibrillation cardiac arrest. Dobutamine infusions (10 micrograms.kg-1.min-1 in 14 animals or 5 micrograms.kg-1.min-1 in 5 animals) begun 15 minutes after resuscitation were compared with controls receiving no treatment (8 animals). The marked deterioration in systolic and diastolic left ventricular function seen in the control group after resuscitation was ameliorated in the dobutamine-treated animals. Left ventricular ejection fraction fell from a prearrest 58 +/- 3% to 25 +/- 3% at 5 hours after resuscitation in the control group but remained unchanged in the dobutamine (10 micrograms.kg-1.min-1) group (52 +/- 1% prearrest and 55 +/- 3% at 5 hours after resuscitation). Measurement of the constant of isovolumic relaxation of the left ventricle (tau) demonstrated a similar benefit of the dobutamine infusion for overcoming postresuscitation diastolic dysfunction. The tau rose in the controls from 28 +/- 1 milliseconds (ms) prearrest to 41 +/- 3 ms at 5 hours after resuscitation whereas it remained constant in the dobutamine-treated animals (31 +/- 1 ms prearrest and 31 +/- 5 ms at 5 hours after resuscitation). CONCLUSIONS: Dobutamine begun within 15 minutes of successful resuscitation can successfully overcome the global systolic and diastolic left ventricular dysfunction resulting from prolonged cardiac arrest and cardiopulmonary resuscitation.

Animals↗
PubMed2006

Early detection of left ventricular diastolic dysfunction in Chagas' disease.

BACKGROUND: Chagas' disease may cause left ventricular diastolic dysfunction and its early detection in asymptomatic patients would allow to stratify the risk and to optimize medical treatment. The aim of this study is to investigate if transmitral Doppler flow can detect early abnormalities of the diastolic left ventricular function in patients during the indeterminate phase of Chagas' disease, in which the electrocardiogram (ECG), chest x-ray and 2-D echocardiogram (2D-echo) are normal. METHODS: a group of 54 patients with Chagas' disease was studied and compared to a control group of 27 subjects of similar age. All were assessed with an ECG, chest X-ray, 2-D echo, and transmitral Doppler flow. RESULTS: both groups had similar values in the 2D-echo. In patients with Chagas' disease, the transmitral Doppler showed a higher peak A velocity (control group: 0.44 m/sec, Chagas group: 0.55 m/sec, p = 0.001), a lower E/A ratio (control group: 1.45, Chagas group: 1.22, p < 0.05), and a lengthening of the deceleration time of early diastolic filling (control: 138.7 +/- 26.8 msec, Chagas group: 167.9 +/- 34.6 msec, p = 001), thus revealing an early disorder of the diastolic left ventricular function in patients with Chagas' disease. CONCLUSION: in patients with Chagas' disease who are in the indeterminate phase, transmitral Doppler flow allowed to identify early abnormalities of the left ventricular diastolic function, which provide useful clinical information for prognostic stratification and treatment.

Adult↗
PubMed1993

Effects of brief repetitive ischemia on contractility, relaxation, and coronary flow. Exaggerated postischemic diastolic dysfunction in pressure-overload hypertrophy.

The recovery of systolic and diastolic function during unstable angina may be modified by the repetition of brief episodes of ischemia and by the presence of left ventricular hypertrophy (LVH). We studied the effects of six consecutive 5-minute cycles of no-flow ischemia and reperfusion followed by 25 minutes of recovery in isovolumic red blood cell-perfused hearts from aortic-banded rats with chronic LVH (n = 8) and sham-operated control rats (n = 8). At baseline (left ventricular end-diastolic pressure [LVEDP], 10 mm Hg), left ventricular developed pressure (123 +/- 5 versus 114 +/- 5 mm Hg/g) and coronary flow [2.5 +/- 0.3 versus 2.2 +/- 0.2 (mL/min)/g] were similar in LVH versus control rats. Repetitive ischemia was associated with progressive depression of postischemic recovery of left ventricular systolic function, and the recovery of left ventricular developed pressure after the final 25-minute reperfusion period was similar in LVH versus control rats (61 +/- 6% versus 72 +/- 4% of baseline, P = NS). Although there was no increase in isovolumic LVEDP during the initial cycle of transient ischemia, both groups showed a rapid and similar rise in LVEDP during subsequent ischemic cycles (delta 82 +/- 8 versus delta 89 +/- 7 mm Hg/g in response to the final ischemia cycle for LVH versus control rats, respectively; P = NS). The control hearts showed complete restoration of LVEDP to baseline during final reperfusion, whereas the LVH hearts showed prolonged and severe postischemic diastolic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

[Observation of enalapril on treating the patients with left ventricular diastolic dysfunction].

The effects of enalapril on 50 patients with left ventricular diastolic dysfunction (LVDD), confirmed by clinical features and radionuclid ventriculography, were assessed in a randomized, double-blind, and controlled method for eight weeks. The results showed that left atrial diameters (LAD), interventricular septum thicknesses (IVST) and left ventricular mass indexes (LV-MI) except left ventricular diameters (LVD) were decreased in the enalapril treatment group. The left ventricular diastolic function parameters such as the early peak filling velocity (EPAV), the atrial peak filling velocity (APAV), the deceleration of early peak filling velocity (DC) and the isovolumic relaxation time (IRT) were improved, the NYHA class and the exercise tolerance were increased, the left ventricular ejection fraction (LVEF), and the cardiac index (CI) were not altered in the enalapril treatment group. The patients with LVDD were well tolerated with enalapril. The parameters mentioned above were not altered in control group. It is suggested that enalapril is an effective drug in the treatment of LVDD.

Adult↗
PubMed1992

Diastolic dysfunction in pressure-overload hypertrophy and its modification by angiotensin II: current concepts.

Cardiac hypertrophy is an adaptive response to an increased load imposed on the myocyte which allows the heart to perform increased work while maintaining normal myocardial fiber stress and shortening in systole. A deleterious consequence of pressure-overload hypertrophy is the prolongation of Ca(2+)-sensitive force inactivation (impaired myocardial relaxation) which is related to intrinsic alterations in cytosolic Ca2+ transport and reuptake in diastole. Additional factors appear to adversely modify myocardial relaxation in the hypertrophied heart, including the imposition of ischemia. There is also evidence that the expression and activity of the cardiac tissue renin angiotensin system (RAS) may be modified in the hypertrophied heart and contribute to diastolic dysfunction. Recent studies have demonstrated the presence of increased cardiac angiotensin converting enzyme (ACE) mRNA expression and activity in animal models of hypertrophy, including the aortic-banded rat with compensatory pressure-overload hypertrophy and rats with post-infarction remodeling. In the beating, isovolumic aortic-banded rat heart, the increased intracardiac activation of angiotensin I to II has been shown to be associated with a dose-dependent depression of diastolic relaxation. Preliminary studies suggest that the depression of diastolic function by angiotensin II in the hypertrophied heart can be prevented by the specific inhibition of cardiac ACE. In addition, the well-recognized susceptibility of the hypertrophied heart to severe ischemic diastolic dysfunction also appears to be favorably modified by the inhibition of cardiac ACE activity. The mechanisms responsible for the adverse effects of angiotensin II on diastolic relaxation in the hypertrophied heart are likely to be complex.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed2006

Diastolic dysfunction in stunned myocardium: a state of abnormal excitation-contraction coupling that is limited by Na+-H+ exchange inhibition.

OBJECTIVE: The systolic and diastolic effects of myocardial stunning were studied to evaluate the contributions of the endocardial and epicardial segments of the ventricular myocardial band, and determine if preconditioning by Na+-H+ exchange (NHE) inhibition effected post-stunning dysfunction. METHODS: Thirteen Yorkshire-Duroc pigs (27.3-38.2 kg) underwent 15 min of mid-LAD clamping. Seven had no protective measures and six were pretreated with IV Cariporide 5 mg/kg 15 min before ischemia. Sonomicrometer crystals evaluated systolic dysfunction (impaired regional shortening) and diastolic dysfunction (contraction extending into early diastole). RESULTS: Before ischemia, contraction started first on the endocardial side followed 82+/-23 ms later by the subepicardium. Endocardial shortening stopped first, coinciding with negative dP/dt onset, while epicardial shortening phase persisted for 92+/-33 ms more during occurrence of rapid LVP descent and development of peak negative dP/dt. Ischemia produced paradoxical bulging of both segments. Sixty minutes after ischemia systolic segment shortening recovered 36+/-24% of baseline values without pretreatment, compared to 75.8+/-15% with Cariporide (p<0.05). Global ejection force (maximum dP/dt) fell 32+/-20% in the unprotected group, but was maintained by Cariporide pretreatment. Diastolic dysfunction always showed continued endocardial contraction into early diastole (occupying 38+/-16% of diastole in untreated hearts), whereas Cariporide treatment reduced this dysfunction to 5+/-10% (p<0.05). Persistent diastolic dysfunction raised left ventricle end diastolic pressure (LVEDP) 4 mmHg in untreated hearts, whereas Cariporide returned LVEDP to normal. Less elevation of creatine kinase MB (CK-MB) and conjugated dienes followed Cariporide pretreatment. CONCLUSIONS: Temporary LAD ischemia alters the normal sequential pattern of contraction responsible for ejection and suction by (a) reducing systolic contractile force, and (b) prolonging endocardial contraction into early diastole to disrupt the normal endocardial-epicardial sequence responsible for ventricular suction. NHE inhibition before ischemia limits postischemic systolic and diastolic dysfunction by re-establishing the expected shortening sequences within the ventricular myocardial band model.

Animals↗
PubMed1995

[Left ventricular diastolic dysfunction in patients with angina decubitus].

Our study population consisted of three groups: 1. 24 cases with ejection fraction (EF) > 45% in 26 patients with angina decubitus (AD) were studied as group A. 2. 20 patients had coronary artery disease without AD as group B. Group B and A were matched for age, EF and coronary artery obstructive lesions. 3. 20 cases without cardiovascular diseases as group C. Left ventriculography (LVG) was performed in these patients. The results showed that left ventricular (LV) early 1/3 filling fraction (1/3FF) was significantly reduced in group A as compared with that in group B and C (both P < 0.001). The findings suggest that patients with AD have abnormalities of LV diastolic filling. Left ventricular end diastolic pressure (LVEDP) significantly increased in patients with AD after LVG as compared with before LVG (P < 0.01). However, there was no statistically difference in LVEDP before and after LVG in both group B and C, indicating that the compliance of LV was also decreased in patients with AD. The increase of LV volume after recumbency would cause increase of LV wall tension and myocardial contraction and aggravate the LV diastolic dysfunction, resulting in a progressive increase in myocardial oxygen consumption. Therefore, we consider that on the basis of severe coronary artery obstructive lesions, LV diastolic dysfunction is a significant pathologic factor in the pathogenesis of AD.

Adult↗
PubMed2003

[Myocardial interstitial fibrosis and diastolic dysfunction in hypertrophic cardiomyopathy].

Hypertrophic cardiomyopathy is an autosomal dominant disease characterized by asymmetrical left ventricular hypertrophy, myocyte disarray, interstitial fibrosis, and small vessel disease. More than 100 mutations in 10 genes, all encoding for sarcomeric proteins, have been identified as responsible for this disease. While the etiology of hypertrophic cardiomyopathy has been extensively elucidated, its pathogenesis is not completely understood. Mutated proteins are incorporated in the sarcomere and impair myocyte contractility. This probably triggers the compensatory local release of trophic factors, which influence the development of the typical anatomical features of the disease. Modifying genes or the effect of environmental or local factors is likely to play a role. Interstitial fibrosis is a morphological characteristic of hypertrophic cardiomyopathy and, increasing chamber stiffness, is an important determinant of diastolic dysfunction. Studies on transgenic animals with hypertrophic cardiomyopathy emphasize the role of interstitial fibrosis in this disease. Recently our group has shown that collagen turnover, evaluated through serum markers of collagen metabolism, is more active in patients with hypertrophic cardiomyopathy than in normal subjects and that patients with passive diastolic dysfunction accumulate collagen I. These studies are potentially relevant as they allow to assess the effects of therapy with cardioreparatory drugs.

Cardiomyopathy, Hypertrophic↗
PubMed1992

Left ventricular diastolic dysfunction in coronary artery disease: effects of coronary revascularization.

Left ventricular diastolic dysfunction was studied globally and regionally in patients with coronary artery disease, and the effects of coronary revascularization were evaluated. A total of 25 patients with angina pectoris who had a stenotic lesion (greater than or equal to 90%) in only left anterior descending branch underwent coronary revascularization [percutaneous transluminal coronary angioplasty (PTCA) in 13 patients and coronary artery bypass graft (CABG) in 12]. Nine patients with normal coronary artery were studied as controls. Left ventricular volume and radial axes were measured on serial frames of one cardiac cycle by cine left ventriculography. The radial axes were drawn from the left ventricular gravity to left ventricular wall at every 20 degrees. Left ventricular filling fraction and distension rate of radial axes were calculated at the times of 25%, 50%, 75%, and 100% of diastolic period, 100% being end-diastole. Although there were no significant changes of the systolic function by revascularization, the filling fraction increased from 11.2 +/- 2.6 to 14.5 +/- 3.5% (p less than 0.001) at 25% time of diastole, from 29.9 +/- 4.9 to 32.5 +/- 5.0% (p less than 0.05) at 50% time in the PTCA group, and from 11.8 +/- 3.7 to 13.4 +/- 3.8% (p less than 0.01) at 25% time in the CABG group. The distension rate of radial axis to the anterior wall also increased significantly at 25% and 50% time of diastole after revascularization, and the change was marked in the PTCA group. However, these increases did not apply to the control patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗