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PubMed1993

Diastolic dysfunction as a cause of heart failure.

Diastolic dysfunction is an important cause of symptoms in patients with various types of cardiac disease. Increased left ventricular diastolic pressure may lead to pulmonary congestion, even in the setting of normal left ventricular systolic function. Although the physiology of diastolic function is complex, left ventricular diastolic pressure may become elevated through one of three broad mechanisms. Abnormalities intrinsic to the left ventricle may include 1) impaired left ventricular relaxation, a finding that is common in most cardiac diseases and may be particularly important during ischemia; 2) increased left ventricular wall thickness relative to cavity volume, which will shift the diastolic pressure-volume relation such that the same volume is associated with a higher pressure; and 3) increased myocardial stiffness, which is thought to be associated with interstitial fibrosis or scar tissue formation. In addition, diastolic pressures may become elevated because of factors extrinsic to the left ventricle. These may include 1) increased central blood volume, which will increase left ventricular pressure without altering the left ventricular pressure-volume relation; and 2) ventricular interaction mediated by pericardial restraint, which may cause a parallel upward shift of the diastolic pressure-volume relation. Treatment of the factors extrinsic to the left ventricle tends to be much more successful than treating abnormalities that are intrinsic to the ventricle. Improved understanding of myocardial relaxation at the cellular level and delineation of the molecular regulation of myocyte hypertrophy and fibroblast proliferation may lead to new and innovative approaches to the treatment of heart failure.

Animals↗
PubMed1992

Comparison of simultaneous Doppler echo and apexcardiogram in detecting left ventricular diastolic dysfunction in patients with systemic hypertension.

Patient with systemic hypertension have often abnormalities of left ventricular (LV) diastolic function. Although pulsed Doppler echocardiography (PDE) is at present time the only simple widely used noninvasive method for evaluating such LV diastolic dysfunction, LV apexcardiogram (ACG) reflecting LV pressure curve changes can also be useful for evaluating LV diastolic events. In order to compare the validity of these two methods in assessing LV diastolic dysfunction, PDE and ACG were simultaneously obtained in 29 patients with chronic systemic hypertension and in 61 controls. As diastolic indices of PDE served the peak early (E) and late atrial (A) diastolic transmitral flow velocities, the A/E ratio and the deceleration time; and of the ACG the relative A-wave to total height (A/H), the total relaxation time (TART), the heart rate corrected TART and the combined index DATI (= diastolic amplitude time index). In patients with hypertension, from the PDE only A and A/E ratio were significantly different from the controls, whereas all mentioned ACG indices showed an abnormal mean value. Thus, the less widely used ACG appears to be a more accurate method in the noninvasive evaluation of diastolic mechanical events than the routinely used PDE in patients with chronic hypertension.

Chronic Disease↗
PubMed2001

Effects of verapamil in normal elderly individuals with left ventricular diastolic dysfunction.

Treatment with oral verapamil for 3 to 4 days has been found to enhance left ventricular (LV) diastolic filling in elderly subjects as assessed by radionuclide angiography. However, there are no Doppler echocardiographic studies to assess the long-term effect of verapamil in normal elderly subjects. Thirteen healthy elderly subjects (mean age, 64 +/- 7 years; 8 men and 5 women) with LV diastolic dysfunction underwent this placebo-controlled cross-over trial. The effect of verapamil on LV diastolic function was assessed by treadmill exercise test and Doppler echocardiography at baseline, and after each 3-month treatment period (placebo or verapamil 120 mg once daily), separated by a 1-week washout period before cross-over. Blood pressure, heart rate, LV ejection fraction, LV mass, and cardiac output were unaltered by placebo or verapamil. The exercise time was similar at baseline (11.4 +/- 2.4 min) and after placebo treatment (11.4 +/- 2.3 min) but significantly increased (P < 0.05) after verapamil treatment (12.3 +/- 2.0 min). The ratio of mitral A wave duration/pulmonary venous atrial systolic reversal duration increased after verapamil treatment (1.12 +/- 0.08) compared to placebo (0.93 +/- 0.06, P < 0.05) and baseline (0.89 +/- 0.09), which had similar durations. The isovolumic relaxation time (IVRT) was significantly decreased (P < 0.05) from 85 +/- 13 msec at baseline and 87 +/- 13 msec with placebo to 73 +/- 9 msec with verapamil. The results of this study suggest that in normal elderly patients with Doppler evidence of diastolic dysfunction, 3 months treatment with verapamil can increase exercise tolerance and improve LV diastolic function.

Aged↗
PubMed1997

Role of MgADP in the development of diastolic dysfunction in the intact beating rat heart.

Sarcomere relaxation depends on dissociation of actin and myosin, which is regulated by a number of factors, including intracellular [MgATP] as well as MgATP hydrolysis products [MgADP] and inorganic phosphate [Pi], pHi, and cytosolic calcium concentration ([Ca2+]c). To distinguish the contribution of MgADP from the other regulators in the development of diastolic dysfunction, we used a strategy to increase free [MgADP] without changing [MgATP], [Pi], or pHi. This was achieved by applying a low dose of iodoacetamide to selectively inhibit the creatine kinase activity in isolated perfused rat hearts. [MgATP], [MgADP], [Pi], and [H+] were determined using 31P NMR spectroscopy. The [Ca2+]c and the glycolytic rate were also measured. We observed an approximately threefold increase in left ventricular end diastolic pressure (LVEDP) and 38% increase in the time constant of pressure decay (P < 0.05) in these hearts, indicating a significant impairment of diastolic function. The increase in LVEDP was closely related to the increase in free [MgADP]. Rate of glycolysis was not changed, and [Ca2+]c increased by 16%, which cannot explain the severity of diastolic dysfunction. Thus, our data indicate that MgADP contributes significantly to diastolic dysfunction, possibly by slowing the rate of cross-bridge cycling.

Adenosine Diphosphate↗
PubMed2002

Progression of systolic abnormalities in patients with "isolated" diastolic heart failure and diastolic dysfunction.

BACKGROUND: The definition of diastolic heart failure (DHF) relies on the use of sensitive tools to exclude the presence of systolic dysfunction. The use of ejection fraction (EF) of 50% as the cutoff point may not be adequate to address such a task. We believe that systolic dysfunction is common in DHF. METHODS AND RESULTS: Echocardiography with tissue Doppler imaging was performed in 339 subjects, of whom 92 had systolic heart failure (SHF) (EF<50%), 73 had DHF (EF > or = 50% with diastolic abnormalities on Doppler echocardiography), and 68 had isolated diastolic dysfunction (DD); 106 were normal control subjects. Regional myocardial velocity curves were constructed off-line with the use of a 6-basal, 6-midsegmental model. The peak regional myocardial sustained systolic (S(M)) and early diastolic (E(M)) velocities were significantly lower in patients with SHF, DHF, and DD than in control subjects in almost all the myocardial segments. Likewise, the mean S(M) (SHF<DHF<DD<control subjects; 3.3 plus/minus 1.0 < 4.6 plus/minus 1.3 < 5.4 plus/minus 1.0 < 6.3 plus/minus 1.0 cm/s; all P less-than-or-equal 0.001) and mean E(M) (SHF=DHF<DD<control subjects; 3.6 plus/minus 1.2 =3.9 plus/minus 1.3 < 5.3 plus/minus 1.6 < 7.2 plus/minus 1.7 cm/s; all P<0.001) from the six basal segments were decreased in all the disease groups. A mean S(M) of 4.4 cm/s (-2 SD of control subjects) predicted the presence of systolic dysfunction in 92% of patients with SHF, 52% with DHF, and 14% with DD. CONCLUSIONS: Through the use of tissue Doppler imaging, systolic abnormalities were evident in patients previously labeled as DHF and to a much lesser extent, isolated DD. This indicates the common coexistence of systolic and diastolic dysfunction in a spectrum of different severity in the pathophysiological process of heart failure.

Aged↗
PubMed1999

Diastolic dysfunction and collagen structure in canine pacing-induced heart failure.

Heart failure is characterized not only by systolic, but also by diastolic dysfunction. The present study tested whether or not diastolic dysfunction is associated with changes in tissue properties and collagen network structure. Heart failure was induced in seven chronically instrumented, conscious dogs by rapid left ventricular pacing (2 50 min(-1)). After 2-5 [mean: 4+/-1 (S.D.)] weeks pacing, heart failure was apparent from clinical symptoms (ascites, cachexia, edema, exercise intolerance) and hemodynamic parameters (significant increases of heart rate and left ventricular end-diastolic pressure and decreases of left ventricular maximal pressure, dP/dtmax and systolic wall thickening). The left ventricle was dilated, as indicated by a decrease of end-diastolic wall thickness (6.3+/-2.0 v 7.2+/-2.1 mm; P<0.05; sonomicrometry). The left ventricular end-diastolic pressure-strain relation (strain: relative change of end-diastolic wall thickness) was obtained during alterations of loading conditions by inferior caval vein and descending thoracic aortic occlusion. The slope of this relation increased from 85+/-20 to 428+/-188 in heart failure, indicating an increase of left ventricular stiffness. Collagen was stained with picrosirius red and analyzed using polarized light microscopy. In heart failure, the collagen volume fraction remained unchanged (1.9+/-1.2 v 2.3+/-1.3%; N.S.), while the nonuniformity of collagen orientation, as reflected by its standard deviation, was increased (11.1+/-1.8 v 6.1+/-0.4 o; P<0.05). The nonuniformity of collagen fiber orientation correlated with left ventricular stiffness [r=0.75].

Animals↗
PubMed1993

Discrepancy between systolic and diastolic dysfunction of the left ventricle in patients with Duchenne muscular dystrophy.

To assess the systolic and diastolic dysfunction of the left ventricle (LV) in relation to age and the severity of impairment in Duchenne muscular dystrophy (DMD), we performed M-mode, two-dimensional and pulsed-wave Doppler echocardiography in 45 male subjects with DMD aged 8 to 25 years and in 40 age-matched healthy controls. Systolic dysfunction started in the first decade of life, with some patients showing severe systolic dysfunction in their early teens. This dysfunction, however, did not always depend on the severity of the skeletal muscle disease. No patients with DMD showed an increase in peak atrial velocity and time-velocity integrals of the atrial contraction velocity curve, findings frequently reported to precede the abnormalities in many cardiac diseases; it was thought therefore that these patients had no increase in left atrial compensation. Diastolic dysfunction may not routinely precede or accompany the systolic dysfunction in DMD, in contrast with what is reported in patients with ischaemic or hypertensive heart disease. DMD patients usually show a predominant systolic dysfunction.

Adolescent↗
PubMed2002

Transforming growth factor-beta function blocking prevents myocardial fibrosis and diastolic dysfunction in pressure-overloaded rats.

BACKGROUND: Excessive myocardial fibrosis impairs cardiac function in hypertensive hearts. Roles of transforming growth factor (TGF)-beta in myocardial remodeling and cardiac dysfunction were examined in pressure-overloaded rats. METHODS AND RESULTS: Pressure overload was induced by a suprarenal aortic constriction in Wistar rats. Fibroblast activation (proliferation and phenotype transition to myofibroblasts) was observed after day 3 and peaked at days 3 to 7. Thereafter, myocyte hypertrophy and myocardial fibrosis developed by day 28. At day 28, echocardiography showed normal left ventricular fractional shortening, but the decreased ratio of early to late filling velocity of the transmitral Doppler velocity and hemodynamic measurement revealed left ventricular end-diastolic pressure elevation, indicating normal systolic but abnormal diastolic function. Myocardial TGF-beta mRNA expression was induced after day 3, peaked at day 7, and remained modestly increased at day 28. An anti-TGF-beta neutralizing antibody, which was administered intraperitoneally daily from 1 day before operation, inhibited fibroblast activation and subsequently prevented collagen mRNA induction and myocardial fibrosis, but not myocyte hypertrophy. Neutralizing antibody reversed diastolic dysfunction without affecting blood pressure and systolic function. CONCLUSIONS: TGF-beta plays a causal role in myocardial fibrosis and diastolic dysfunction through fibroblast activation in pressure-overloaded hearts. Our findings may provide an insight into a new therapeutic strategy to prevent myocardial fibrosis and diastolic dysfunction in pressure-overloaded hearts.

Animals↗
PubMed2000

Diastolic dysfunction in patients with congenital heart disease.

As noted in the introduction of this article, a comprehensive evaluation of diastolic function in all known congenital heart defects is not feasible; however, by demonstrating several representative anatomic and genetic abnormalities where diastolic dysfunction may have clinical significance, it is hoped that scaffolding has been established which will provide structure for further study on this intriguing and influential component of function in patients with CHD. Understanding the contribution of diastole to overall ventricular function may be shown to have important implications in the recommendations for timing or potential benefit of surgical intervention. Or, to state differently, if diastolic dysfunction precedes that of systolic, would a rigorous analysis of diastole in the presurgical patient provide a more sensitive algorithm for intervention? The means for noninvasive assessment of diastolic function, primarily by spectral Doppler echocardiography, or using echocardiography in conjunction with other modalities, should allow for a comprehensive accrual of data in this patient population.

Diastole↗
PubMed1989

Diastolic dysfunction of perfused rat hearts induced by hydrogen peroxide. Protective effect of selenium.

Oxidant substances such as hydrogen peroxide are postulated to cause cardiac dysfunction and injury in a number of pathological conditions. Selenium is an essential nutrient which serves as an oxidant defense through the selenoenzyme glutathione peroxidase. This enzyme metabolizes hydrogen peroxide; its activity in rat heart is reduced to 5% of control by selenium deficiency. Left ventricular function of selenium-deficient and control rat hearts was studied in a Langendorff preparation under isovolumic conditions. A stabilization period of 20 min was followed by a 70 min infusion of hydrogen peroxide at 375 or 1500 nmol/min. When no hydrogen peroxide was infused, perfusion for 90 min had no effect on systolic or diastolic function and no effect of selenium deficiency was detected. Hydrogen peroxide infusion into selenium-deficient hearts at 375 nmol/min led to impaired isovolumic relaxation and a substantial increase in end-diastolic pressure after 45 min which worsened progressively until the experiment was terminated. By contrast no effect was observed on systolic contractile function as assessed by peak pressure or developed pressure. Infusion of this dose of hydrogen peroxide into control hearts had no significant effect on diastolic or systolic function. However, infusion of 1500 nmol hydrogen peroxide/min into control hearts caused diastolic dysfunction after 30 min without affecting systolic function. These results indicate that hydrogen peroxide injury to the perfused rat heart is manifested by diastolic dysfunction before systolic dysfunction occurs. Selenium deficiency lowers the dose of hydrogen peroxide needed to cause diastolic dysfunction. This suggests that the selenoenzyme glutathione peroxidase protects the heart against hydrogen peroxide injury.

Animals↗
PubMed2000

Worsening of left ventricular diastolic dysfunction during exercise causes decreased exercise tolerance in hypertension.

BACKGROUND: Exercise tolerance is reduced in hypertension. Hypertension affects left ventricular (LV) diastolic filling by causing abnormal relaxation and decreasing compliance. HYPOTHESIS: This study was designed to determine whether worsening of LV diastolic dysfunction during exercise causes decreased exercise tolerance in hypertension. METHODS: Left ventricular diastolic filling parameters were examined at mitral valve by Doppler echocardiography at rest and at peak exercise in hypertensive patients and were compared with those of age- and gender-matched normotensive individuals. Treadmill exercise stress test was performed according to the Bruce protocol and the exercise time was recorded. RESULTS: Exercise time was significantly shorter in the hypertensive group than that in the normotensive group (320 +/- 29 vs. 446 +/- 38 s, p 0.03). The hypertensive group demonstrated abnormal relaxation pattern of diastolic mitral inflow at rest, which became pseudonormal at peak exercise (E/A velocity ratio, rest 0.86 +/- 0.06 vs. exercise 1.19 +/- 0.09, p < 0.001). The diastolic mitral inflow pattern remained normal at peak exercise in the normotensive group. The deceleration time and the pressure half time of early mitral inflow at peak exercise were significantly shorter in the hypertensive group than those in the normotensive group (deceleration time, 182 +/- 20 vs. 238 +/- 22 ms, p 0.02: pressure half time, 54 +/- 5 vs. 70 +/- 12 ms, p 0.01). CONCLUSIONS: This study demonstrates that reduced exercise tolerance in hypertension is associated with worsening of diastolic dysfunction during exercise consistent with an increase in left atrial pressure.

Compliance↗
PubMed1995

Is diastolic dysfunction associated with thrombogenesis? A study of circulating markers of a prothrombotic state in patients with coronary artery disease.

Clinical data on the contributory role of heart failure to thromboembolic risk does not differentiate between systolic and diastolic left ventricular dysfunction. We therefore conducted a population-controlled cross-sectional study to determine levels of plasma fibrinogen (associated with thromboembolism), fibrin D-dimer (a marker of fibrin turnover) and von Willebrand factor (a marker of endothelial dysfunction) in patients with ischaemic heart disease (a common cause of diastolic dysfunction) in whom left ventricular diastolic function was defined by echocardiography. We studied 106 patients: those with normal left ventricular function (n = 42, Group 1); those with left ventricular dysfunction but without aneurysms (n = 34, Group 2); and those with left ventricular aneurysm formation (n = 30, Group 3). Each of these groups was subdivided into those with (a) and without (b) diastolic dysfunction. Diastolic dysfunction was present in over 60% of patients, irrespective of left ventricular systolic impairment. There were no significant differences in median levels of plasma fibrinogen, fibrin D-dimer or von Willebrand factor in each group of patients with ischaemic heart disease, whether or not left ventricular diastolic dysfunction was present (Mann-Whitney test; P = N.S.). Systolic (rather than diastolic) dysfunction was the main correlate of these (analysis of variance, general linear model--ANOVA-GLM--P < 0.05) and the greatest abnormalities of fibrinogen, endothelial dysfunction and intravascular fibrin turnover were seen in patients with left ventricular aneurysms whether or not diastolic dysfunction was present. This study demonstrates that there is no evidence of a significant additional contribution to thrombotic risk (as assessed by plasma fibrinogen, von Willebrand factor and fibrin D-dimer) for patients with left ventricular diastolic dysfunction. A relationship is noted between some prothrombotic factors and Doppler indices of flow, which suggests a possible association between cardiac haemodynamics and thrombogenesis.

Analysis of Variance↗
PubMed1998

Diastolic dysfunction coincides with early mild transplant rejection: in situ measurements in a heterotopic rat heart transplant model.

BACKGROUND: Diastolic dysfunction seen in early clinical transplant rejection has been difficult to demonstrate in experimental rodent models because of the inability to make sensitive in situ measurements of systolic and diastolic functions. We have developed a heterotopic heart transplant model with Fisher 344 and ACI rats (without immunosuppression), where in situ measurements of diastolic and systolic functions were made sequentially (daily) by use of an implanted left ventricular balloon. METHODS: Syngeneic and allogeneic heterotopic heart transplants were performed. In situ function was determined by varying balloon volume to measure the developed pressure, the rates of pressure rise (+dp/dt) and pressure fall (-dp/dt), diastolic pressure-volume relationship, and the time constant of diastolic relaxation (tau). These results were compared with function measurements in transplanted hearts that were excised and perfused in a Langendorff mode (ex vivo) during the same posttransplantation period. RESULTS: Histologic examination revealed that at day 3 after transplantation, allografts showed mild lymphocytic infiltration indicative of mild or early rejection, and by day 5, there was severe rejection with myocyte necrosis. By day 3, the slope of the diastolic pressure-volume relationship (ie, left ventricular stiffness) was significantly higher in allografts as compared with isografts (436 +/- 96 vs 177 +/- 26 mm Hg/mL, p < .05). Similarly, tau was significantly longer in allografts by day 3 after transplantation. Developed pressure and +dp/dt became significantly lower in allografts beginning on day 6. Function measurements made in the isolated perfused ex vivo hearts yielded the same results at day 3 after transplantation as the in situ group of hearts. CONCLUSION: Using a chronically implanted left ventricular balloon, we have developed a heterotopic heart transplant model where sensitive measurements of systolic and diastolic functions can be made. With this preparation, the early changes in the diastolic dysfunction seen clinically can be reproducibly detected. Thus this model may be useful to study mechanisms and interventions during early transplant rejection.

Animals↗
PubMed1991

Left ventricular diastolic dysfunction presenting as ascites: the importance of clinically assessing central venous pressure.

A 66-year-old man without history of heart disease or symptoms of left ventricular (LV) failure was admitted with transudative ascites. Echocardiography showed no valvular or pericardial disease and normal LV function. Gated pool scintigraphy confirmed normal LV systolic function but demonstrated severe right ventricular systolic dysfunction. Catheterization revealed left ventricular diastolic dysfunction as the cause of right-sided failure. The clinician evaluating transudative ascites cannot exclude LV failure on the basis of noninvasive assessment of systolic function alone. Appreciation of an elevated central venous pressure remains the most important evidence of a cardiac source of ascites.

Aged↗
PubMedDate not supplied

Allograft diastolic dysfunction and chronotropic incompetence limit cardiac output response to exercise two to six years after heart transplantation.

BACKGROUND: Because prolonged survival of heart transplant recipients is expected with the current immunosuppressive treatment, the functional capacity of these long-term survivors is of interest. Previous exercise studies showed no objective improvement in exercise tolerance several years after transplantation, but the extent to which chronotropic incompetence and allograft diastolic dysfunction observed early after transplantation may improve over time has not been defined. METHODS: Thirteen untrained heart transplant recipients without symptoms, between 27 and 70 months after transplantation, and 13 age-matched sedentary normal controls underwent maximal upright bicycle exercise testing with simultaneous hemodynamic, radionuclide, and expired gas measurements. RESULTS: Systolic function as measured by ejection fraction was supranormal at rest in the transplant group and normalized with exercise. Despite their maximal exercise effort, transplant recipients had a 60% reduction in their exercise capacity compared with nontransplant recipients. Peak oxygen consumption was similarly reduced by 52%. Cardiac output response to exercise was 43% lower in the transplant group because of a 78% reduction in heart rate reserve and an 18% reduction in maximal stroke volume. Ventricular volumes were similarly reduced after transplantation, but filling pressures remained normal, indicating allograft diastolic dysfunction. Despite the significantly reduced maximal cardiac output, maximal arteriovenous oxygen difference was 25% lower in the transplant recipients, suggesting a peripheral deficit in oxygen handling. CONCLUSIONS: Therefore, patients, 2 to 6 years after transplantation, continue to have a significant reduction in exercise tolerance as a result of a combination of severe chronotropic incompetence, limited stroke volume reserve caused by a reduced ventricular size and allograft diastolic dysfunction, and an abnormality in peripheral oxygen delivery or use. Efforts aimed at improving these factors may further enhance the functional capacity of these long-term survivors of heart transplantation.

Cardiac Output↗
PubMed1997

Role of left ventricular hypertrophy in diastolic dysfunction in aged hypertensive patients.

OBJECTIVE: To evaluate the influence of left ventricular hypertrophy (LVH) on the diastolic dysfunction in older hypertensive patients. METHODS: In total 665 patients (58% men, 61% White, aged 55-80 years) with mild-to-moderate essential hypertension underwent Doppler echocardiography. Data included left ventricular dimensions, left ventricular mass index, body mass index, E- and A-wave mitral flow velocities, E:A ratio, deceleration time > 150 ms), impaired relaxation (E:A ratio < 1.0, prolonged deceleration time according to age), and restrictive physiology (E:A ratio > 2.1, deceleration time < 150 ms)]. Data were distributed according to age (50-59, 60-69, and 70-80 years). RESULTS: The overall prevalence of sex-adjusted LVH in this study was 65%. When we compared hypertensive patients with and without LVH, the E- and A-wave velocities, E:A ratio, and deceleration time were similar. Moreover, the prevalences of normal, impaired relaxation, and restrictive physiology patterns among patients with and without LVH did not differ significantly (20, 79.5, and 0.5 versus 24, 75.5, and 0.5%). When the mitral flow patterns were adjusted according to age, the impaired relaxation pattern increased further with age (to 73% during the fifth decade, 83% during the sixth decade, and 88% during the seventh decade). CONCLUSIONS: LVH is not an independent factor associated with abnormal flow patterns in hypertensive patients aged over 50 years with normal systolic contractility. The impaired relaxation is the predominant pattern of diastolic dysfunction in older hypertensive patients and increases further with aging.

Aged↗
PubMedDate not supplied

Left ventricular diastolic dysfunction secondary to hyperglycemia in patients with type II diabetes.

Diabetes mellitus type II, a cause of preclinical left ventricular dysfunction that can progress to cardiac insufficiency ventricular dysfunction in diabetic patients, is attributed to systemic arterial hypertension, or ischemic cardiopathy. Diastolic ventricular dysfunction takes place during the course of diabetes mellitus. The purpose of the present article is to report on the influence of hyperglycemia on the left ventricular diastolic dysfunction independently of dyslipidemia, obesity, and systemic arterial hypertension, usually present in diabetic patients. Left ventricular diastolic function was studied by Doppler echocardiography in asymptomatic type II diabetic patients without ischemic or valvular cardiopathies, cardiomegaly, or systemic arterial hypertension. Two groups of patients were integrated: patients with and without left ventricular diastolic dysfunction, i.e., groups A and B, respectively. Glycemia, cholesterol, triglycerides, and body mass index (BMI) were determined in each subject. Bivariate statistical tests (Student t, chi-square, or Mann-Whitney U tests) were applied to study the influence of the previously mentioned variables on the ventricular diastolic function. To evaluate the influence of hyperglycemia on ventricular diastolic function separately from dyslipidemia, systemic arterial hypertension, and the influence of obesity, logistic regression, and multivariate statistical analysis were applied. Independently of dyslipidemia and obesity, a relationship was found between hyperglycemia and diastolic dysfunction of the left ventricle in patients belonging to group A (p <0.05, odds ratio [OR] 12.1). No statistical significance was found between glycemia and the diastolic function of the left ventricle in group B patients. Even in type II diabetic patients without cardiopathy, uncontrolled hyperglycemia provokes diastolic left ventricular dysfunction.

Adult↗
PubMed1988

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location.

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.

Cardiac Volume↗