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At least 1,639 records · Page 91Linked to original sources
PubMed1993

Endothelin-1 exacerbates diastolic stunning in conscious dogs.

The purpose of this study was to examine the effects of endothelin-1 (ET-1) on "diastolic stunning" in the postischemic myocardium. In 14 conscious dogs receiving either placebo (n = 7) or ET-1 (2.5 ng.kg-1.min-1, n = 7), left ventricular (LV) hemodynamics and regional wall motion (systolic segmental shortening by sonomicrometry and the ischemic-nonischemic regional asynchrony during isovolumic relaxation) were assessed at baseline, during 10 min of left anterior descending coronary artery occlusion (CAO) and at 60 min after reflow (R-60). During CAO, the ischemic segment shortening was severely depressed and both regional asynchrony and LV relaxation time constant were significantly increased in the placebo and ET-1 groups. At R-60, this LV diastolic dysfunction recovered to baseline conditions in the placebo group but was still present in the ET-1 group. Because coronary and myocardial blood flow returned to the baseline level at R-60 in both groups, the deleterious effects of ET-1 on diastolic stunning are probably mediated by its direct action on the myocardium.

Animals↗
PubMedDate not supplied

[Changes in left ventricular diastolic function and in tolerance to physical loading under the influence of finoptin in stenocardia patients].

A total of 45 patients aged 53.6 +/- 6.1 years who had Functional Class II-IV angina pectoris were examined. In patients with stable angina and normal left ventricular diastolic pressure, a moderate antianginal effect of finoptin was shown to be associated with decreased myocardial afterload. The normalizing effects of finoptin on baseline left ventricular diastolic dysfunction along with lower myocardial afterload resulted in an increase in coronary reserve and a more pronounced antianginal effect.

Adult↗
PubMed2003

Morphological and functional alterations in ventricular myocytes from male transgenic mice with hypertrophic cardiomyopathy.

Familial hypertrophic cardiomyopathy (FHC) is a human genetic disorder caused by mutations in sarcomeric proteins. It is generally characterized by cardiac hypertrophy, fibrosis, and myocyte disarray. A transgenic mouse model of FHC with mutations in the actin-binding domain of the alpha-myosin heavy chain (MyHC) gene displays many phenotypes similar to human FHC. At 4 months, male transgenic (TG) mice present with concentric cardiac hypertrophy that progresses to dilation with age. Accompanying this latter morphological change is systolic and diastolic dysfunction. Left ventricular (LV) myocytes from male TG and wild-type (WT) littermates at 5 and 12 months of age were isolated and used for morphological and functional studies. Myocytes from 5- and 12-month-old TG animals had shorter sarcomere lengths compared with WT. This sarcomere length difference was abolished in the presence of 2,3-butanedione monoxime, suggesting that the basal level of contractile element activation was increased in TG myocytes. Myocytes from 12-month-old TG mice were significantly longer than those from age-matched WT controls, and TG myocytes exhibited Z-band disorganization. When cells were paced at 0.5 Hz, TG myocyte relengthening and the fall in intracellular [Ca2+] were slowed when compared with cells from age-matched WT controls. Moreover, an increased amount of beta-myosin heavy chain protein was found in hearts from TG compared with WT. Thus, myocytes from the alpha-MyHC TG mouse model display many morphological and functional abnormalities that may help explain the LV dysfunction seen in this TG mouse model of FHC.

Age Factors↗
PubMed2003

[Arterial hypertension and ischemic heart disease: clinico-echocardiographic aspects].

Doppler M-mode echocardiography was made in 156 males with ischemic heart disease (IHD) verified coronarographically. The patients were normotensive or had mild, moderate and severe arterial hypertension (AH) (groups 1, 2, 3 and 4, respectively). The groups were similar by functional anginal class. Echocardiographic findings were in many cases similar. This supports the hypothesis that IHD and AH are closely related. However, the addition of AH to atherosclerotic affection of the coronary artery or atherosclerosis rise in the presence of AH is associated with development of myocardial hypertrophy which is registered at echocardiography and correlates in severity with severity of AH. Myocardial hypertrophy is, on the one side, compensatory as it prevents dilation of the left ventricle and impairment of its contractility rising at later stage of the disease with depletion of the myocardial and coronary reserves, but, on the other side, it promotes diastolic dysfunction of the left ventricle, lowers its performance. The above phenomena are most pronounced in combination of IHD with severe AH. This combination presents a new qualitative state and, therefore, needs new approaches to its correction.

Adult↗
PubMed2006

Mechanical and metabolic rescue in a type II diabetes model of cardiomyopathy by targeted gene transfer.

The Otsuka-Long-Evans Tokushima Fatty rat represents a model for spontaneous non-insulin-dependent type II diabetes mellitus (DM), characterized by diastolic dysfunction and associated with abnormal calcium handling and decrease in sarcoplasmic reticulum Ca2+ -ATPase (SERCA2a) expression. The aim of this study was to examine whether SERCA2a gene transfer can restore the energetic deficiency and left ventricular (LV) function in this model. DM rats were randomized to receive adenovirus carrying either the SERCA2a gene (DM + Ad.SERCA2a) or the beta-galactosidase gene (DM + Ad.betaGal) or saline (DM + saline). LV mechanoenergetic function was measured in cross-circulated heart preparations 3 days after infection. In DM, end-systolic pressure at 0.1 ml intraballoon water (ESP0.1) was low and end-diastolic pressure at 0.1 ml intraballoon water (EDP0.1) was high (22 mm Hg), compared with non-DM (EDP0.1 12 mm Hg). In DM + Ad.SERCA2a, however, ESP0.1 was increased over 200 mm Hg and EDP(0.1) was decreased to 7 mm Hg. LV relaxation rate was fast in DM + Ad.SERCA2a, but slow in the other DM groups. There was no difference in relation between cardiac oxygen consumption per beat and systolic pressure-volume area among all groups. Finally, the oxygen cost of LV contractility in DM was about three times as high as that of normal. In DM + Ad.SERCA2a, the oxygen cost decreased to control levels, but in DM + Ad.betaGal/DM + saline it remained high. In DM failing hearts, the high oxygen cost indicates energy wasting, which contributes to the contractile dysfunction observed in diabetic cardiomyopathy. SERCA2a gene transfer transforms this inefficient energy utilization into a more efficient state and restores systolic and diastolic function to normal.

Adenoviridae↗
PubMed1998

Molecular aspects of adrenergic signal transduction in cardiac failure.

Abnormal beta-adrenergic signal transduction and intracellular Ca2+ handling appear to be a major cause of systolic and diastolic dysfunction in humans with heart failure. The precise mechanisms which cause an alteration in Ca2+ handling have been a subject of investigation in recent years. Several lines of evidence suggest that activation of neurohormonal systems plays a central role. Altered Ca2+-handling (increased diastolic concentrations, reduced systolic Ca2+ release) have a strong impact on diastolic and systolic performance of failing hearts. Sarcoplasmic reticulum Ca2+ ATPase is reduced in activity and in steady-state mRNA concentration. The Na+-Ca2+ exchanger is upregulated at the mRNA and protein levels. Phospholamban depends strongly on cAMP-dependent phosphorylation. A strong sympathetic activation has been shown to desensitize the cAMP system. At the receptor level, there is downregulation of beta1-adrenergic receptors. An uncoupling of beta2-adrenoceptors has been attributed to an increased activity and gene expression of beta-adrenergic receptor kinase in failing myocardium, leading to phosphorylation and uncoupling of receptors. Finally, recent evidence suggests that cAMP-dependent transcription mechanisms may play a role during beta-adrenergic stimulation and cardiomyopathy with heart failure - by means of altered actions of cAMP response element binding protein, the cAMP response element modulator, or the activating transcription factor 1. The exact characterization of signal transduction defects could offer novel approaches to the pharmacological treatment of heart failure.

Animals↗
PubMed1998

Diagnosis and management of iron-induced heart disease in Cooley's anemia.

Patients with homozygous beta-thalassemia are chronically transfused and, if not assiduously chelated, are at risk for cardiac dysfunction. Available data suggest that even in optimally chelated patients, cardiac pathology is abnormal secondary to iron deposition, fibrosis, hypertrophy, and the structural effects of chronic anemia. Evidence of myopericarditis may also be found. Cardiac performance is usually only subtly affected, primarily with diastolic abnormalities not routinely detected on echocardiograms or nuclear scan. In poorly chelated patients, severe heart failure occurs and is easily predictable but invariably fatal, despite treatment with diuretics, vasodilators, inotropes, and antiarrhythmics. Based on successful prevention of heart failure with ACE inhibitors in other forms of cardiomyopathy, we suggest multicenter trials to explore methods to stabilize cardiac function in patients at risk for iron-induced heart disease. Long-term adverse effects of iron deposition, diastolic dysfunction, and abnormal hormone regulation need to be quantitated in patients reaching their third and fourth decades when the potential for ischemic cardiac disease could compound cardiac dysfunction.

Anemia, Hemolytic↗
PubMed1990

Doppler echocardiographic evaluation of left ventricular diastolic function in adolescents with diabetes mellitus.

Doppler echocardiograms of the mitral valve were recorded along with electrocardiograms and respirations from 20 diabetics and 16 normal subjects, all aged 10 to 15 years. E and A areas (the components of the total velocity-time integral in the early passive period of ventricular filling [E] and the late active period of atrial emptying [A], respectively), the peak E and A velocities (cm/s) and the 1/3 area fraction (or the proportion of filling in the first 1/3 of diastole) were measured. Each of the following was significantly greater for the normal subjects versus diabetic patients: peak E (96 +/- 14 vs 81 +/- 14 cm/s, p less than 0.005), E/total area (0.74 +/- 0.04 vs 0.69 +/- 0.06, p less than 0.005) and peak E/A velocity ratio (2.38 +/- 0.55 vs 1.92 +/- 0.55, p less than 0.05). The mean heart rates and ages were not significantly different for the 2 groups. The remaining parameters (peak A velocity, A/total area, E/A area, and 1/3 area fraction) were also not significantly different for the 2 groups. This study is the first to demonstrate diastolic dysfunction in pediatric patients with diabetes and may indicate abnormalities of ventricular relaxation or compliance in diabetes mellitus.

Adolescent↗
PubMed1991

Relationship between left ventricular end-diastolic compliance and abnormal Doppler mitral filling in patients with coronary artery disease.

Left ventricular end-diastolic compliance (LVEDC) and transmitral flow velocities were measured in 19 patients with coronary artery disease associated with hypertension and 10 normal subjects by LV catheterization and pulsed-Doppler echocardiography. LVEDC was much lower in the patient than in the normal subjects (P less than 0.01). The data showed that abnormal Doppler diastolic function such as elevated late diastolic peak flow velocity (PVA) and decreased LVEDC occurred in the patients at the same time. In addition, the negative correlation of PVA with LVEDC observed in normal controls but not in patients suggested that in patients with impaired diastolic filling, factors other than the decreased LVEDC itself must also participate in the development of diastolic dysfunction.

Aged↗
PubMedDate not supplied

Clinical trials in diastolic heart failure.

Forty percent to 50% of patients with chronic heart failure have normal or relatively normal left ventricular ejections fractions. These are much more frequently women and tend to be older than those with reduced ejection fractions. In most, left ventricular diastolic dysfunction plays a major role in the genesis of heart failure. Until recently, these patients have been systematically excluded from heart failure trials, so that there are no proven treatments for this group. This article reviews the recent and ongoing trials in patients with diastolic heart failure, which hopefully will lead to improved treatment and outcomes.

Adrenergic beta-Antagonists↗
PubMed1979

Right ventricular diastolic pressure in coronary artery disease.

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.

Aortic Valve Stenosis↗
PubMed2003

Time interval between onset of mitral inflow and onset of early diastolic velocity by tissue Doppler: a novel index of left ventricular relaxation: experimental studies and clinical application.

OBJECTIVES: The goal of this study was to examine the diagnostic utility of the time to onset of early (Ea) diastolic velocity of the mitral annulus by tissue Doppler (TD) in comparison with the time to onset of mitral inflow (T(Ea-E)) for the assessment of left ventricular (LV) relaxation. BACKGROUND: Tissue Doppler imaging of the mitral annulus provides useful information about myocardial function. So far, studies have focused on the measurement of peak Ea, but have not evaluated the diagnostic utility of the time to onset of Ea. METHODS: Simultaneous left heart catheterization and Doppler echocardiography (DE) were performed in 10 dogs. Left atrial pressures and LV volumes and pressures were measured before and after constriction of the circumflex (cx) coronary artery. The delay in Ea was next examined in 60 consecutive patients, undergoing simultaneous right heart catheterization and DE. Furthermore, (T(Ea-E)) was used to predict filling pressures in a prospective group of 33 patients. RESULTS: In canine studies, significant prolongation in the time interval (T(Ea-E)) was noted after cx constriction, which had a significant relation with tau (tau) (r = 0.93, p < 0.01). In human studies, Ea was significantly delayed in patients with impaired relaxation and pseudonormal LV filling in comparison with age-matched controls. In the prospective group, pulmonary capillary wedge pressure (PCWP) derived as: PCWP(Doppler) = LV(end-systolic pressure) x e(-IVRT/(T(Ea-E))), where IVRT is isovolumetric relaxation time; PCWP(Doppler) related well to PCWP(catheter) (r = 0.84, p < 0.001). CONCLUSIONS: T(Ea-E) is a useful novel index of LV relaxation. It can be used to identify patients with diastolic dysfunction and predict PCWP.

Aged↗
PubMed1999

Doppler echocardiographic-guided diagnosis and therapy of heart failure.

Abnormalities of diastolic function play a major role in producing the signs and symptoms of heart failure. In patients with heart failure and reduced left ventricular systolic function, concomitant diastolic dysfunction is invariably present. In addition, it is now well established that as many as 40% to 50% of patients with well-documented episodes of heart failure have preserved systolic function. Doppler echocardiography provides one of the most useful clinical tools for assessing left ventricular diastolic function and can provide diagnostic and prognostic information. The Doppler assessment of diastolic function should be part of the routine echocardiographic evaluation of patients suspected of having heart failure. This review focuses on the use of Doppler echocardiographic techniques to assess diastolic function. The Doppler patterns of diastolic filling observed and their progression over time in patients with myocardial disease are described and related to changes in the physiology of diastolic filling. In addition, Doppler echocardiographic-guided treatment strategies for heart failure are discussed.

Aged↗
PubMed1989

Contrasting effects of single doses of pindolol and xamoterol on left ventricular diastolic function.

Impaired left ventricular diastolic dysfunction is common in patients with ischaemic heart failure. The beta 1-adrenoceptor partial agonist xamoterol was compared with pindolol, a beta-adrenoceptor blocker with intrinsic sympathomimetic activity, in a haemodynamic study in 17 patients with ischaemic heart disease. Pindolol caused left ventricular end-diastolic pressure, wall stress and T1 to rise, whereas xamoterol produced improvements in all three parameters. These results suggest that xamoterol may be of greater benefit to patients in heart failure.

Adrenergic beta-Agonists↗
PubMed2004

[The U-wave in ischemia and left ventricular dysfunction after myocardial infarct].

INTRODUCTION: The occurrence of U-wave in electrocardiogram appears after T-wave. It is period of the greatest excitability of the myocardium in heart electrical activity usually of the some direction as its own T-wave. AIM OF THE WORK ANALYSE: U-wave with ischaemia and dysfunction of the myocardium in exercise test. MATERIAL AND METHODS: The prospective study has been done for 51 patients. Electrocardiogram, exercise test vas made for all patients and immediately after test, echocardiography with Doppler and colour-Doppler. In the analysis of dysfunction of the left chamber these important parameters were followed: METS; decrease of blood pressure, devaluation of ST-segment, U-wave, heart rate, dyspnea, sweating and paleness. RESULTS: Positive U-wave was noticed in 51%, negative in 24% examinees. Sensitivity of U-wave on the base of the breakdown of segmental vall motion in echocardiography (ischaemia) is 66.67% with false negative resists of 33.33%. Systolic dysfunction with influential parameters correlates in the best way with decrease of blood pressure and regressive coefficient is 66.93, but the weabest correlation is with U-wave (0.53). Correlative coefficient for U-wave in systolic function is 0.263. Regressive coefficient with influential parameters in diastolic dysfunction is 3.34, correlative coefficient is 0.108. CONCLUSIONS: U-wave in registered at rest after exercise test when heart rate is equal or below 95 in a minute. Registration of U-wave is an additional parameter in diagnostics of ischaemia and dysfunction of the myocardium of the left chamber (small influence).

Echocardiography↗
PubMed1997

Doppler-echocardiography study of cardiac function during a 36 atm (3,650 kPa) human dive.

To determine the influence of a saturation dive on cardiac function, Doppler-echocardiographic measurements were compared at sea level and during a 36 atm (3,650 kPa) He-O2 dive (gas density: 7 g/liter) in four healthy men. Left ventricular systolic function was studied from time motion measurements. Transmitral flow (E:A ratio) and isovolumetric relaxation time were used to assess left ventricular diastolic function. Cardiac output was derived from systolic pulmonary and aortic valvular flows. Cardiac output decreased 4.4 +/- 0.8 vs. 5.9 +/- 1.2 liter/min at sea level) whereas stroke volume, left ventricular ejection fraction, atria and ventricular diameters remained unchanged. Thus, the decrease in cardiac output was attributed to bradycardia (56 +/- 8 vs. 73 +/- 9 beats/min at sea level) which probably resulted from the slight hyperoxia (PI(O2), 0.4 atm). We found no evidence of left ventricular diastolic dysfunction. nor did we find valvular regurgitation or pulmonary hypertension. We conclude that Doppler-echocardiography can be used safely to investigate cardiac function during human saturation dives. Our results suggest that a 36 atm He-O2 dive does not modify cardiac or systolic and diastolic function except for a slight decrease in cardiac output correlated to bradycardia.

Adult↗
PubMed2007

Echocardiographic evaluation of ventricular function in mice.

Ventricular dysfunction remains a hallmark of most cardiac disease. The mouse has become an essential model system for cardiovascular biology, and echocardiography an established tool in the study of normal and genetically altered mice. This review describes the measurement of ventricular function, most often left ventricular function, by echocardiographic methods in mice. Technical limitations related to the small size and rapid heart rate in the mouse initially argued for the performance of echocardiography under anesthesia. More recently, higher frame rates and smaller probes operating at higher frequencies have facilitated imaging of conscious mice in some, but not all, experimental protocols and conditions. Ventricular function may be qualitatively and quantitatively evaluated under both conditions. Particular detail is provided for measurement under conscious conditions, and measurement under conscious and sedated or anesthestized conditions are contrasted. Normal values for echocardiographic indices for the common C57BL/6 strain are provided. Diastolic dysfunction is a critical pathophysiologic component of many disease states, and progress in the echocardiographic evaluation of diastolic function is discussed. Finally, echocardiography exists among several competing imaging technologies, and these alternatives are compared.

Adrenergic Agents↗
PubMed2002

Left ventricular diastolic function in essential hypertensive patients: influence of age and left ventricular geometry.

PURPOSE: To evaluate diastolic dysfunction (DD) in essential hypertension and the influence of age and cardiac geometry on this parameter. METHODS: Four hundred sixty essential hypertensive patients (HT) underwent Doppler echocardiography to obtain E/A wave ratio (E/A), atrial deceleration time (ADT), and isovolumetric relaxation time (IRT). All patients were grouped according to cardiac geometric patterns (NG - normal geometry; CR - concentric remodeling; CH- concentric hypertrophy; EH - eccentric hypertrophy) and to age (<40; 40 - 60; >60 years). One hundred six normotensives (NT) persons were also evaluated. RESULTS: A worsening of diastolic function in the HT compared with the NT, including HT with NG (E/A: NT - 1.38+/-0.03 vs HT - 1.27+/-0.02, p<0.01), was observed. A higher prevalence of DD occurred parallel to age and cardiac geometry also in the prehypertrophic groups (CR). Multiple regression analysis identified age as the most important predictor of DD (r2=0.30, p<0.01). CONCLUSION: DD was prevalent in this hypertensive population, being highly affected by age and less by heart structural parameters. DD is observed in incipient stages of hypertensive heart disease, and thus its early detection may help in the risk stratification of hypertensive patients.

Adult↗