PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Ventricular Dysfunction, Left”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 685 records · Page 38Linked to original sources
PubMed2006

Echocardiography and reversible left ventricular dysfunction.

PURPOSE: Transient apical ballooning is increasingly recognized in acutely ill, hospitalized patients. This article reviews clinical aspects of the syndrome, its recognition by echocardiography, and will review other disorders whose recognition is due primarily to the availability of echocardiography. METHODS: Systematic review of the medical literature concerning the syndrome of transient apical ballooning. RESULTS: Seven recent studies of transient apical ballooning are reviewed; the clinical characteristics, biomarker data, echocardiographic findings, and angiographic data are remarkably similar. Most afflicted individuals are women in their seventh decade who develop chest symptoms in close relationship to a "trigger" event--this is usually either severe emotional distress, a medical illness, or a procedure. CONCLUSIONS: Transient apical ballooning is not uncommonly encountered among acutely ill, hospitalized patients with chest symptoms. As yet there is no consensus of the underlying mechanism, although there is reason to believe that catecholamine injury to the myocardium is partially, if not wholly responsible. The widespread use of echocardiography appears to be responsible for the increasing recognition of this (and other) syndromes.

Catecholamines↗
PubMed2006

Tea catechins improve left ventricular dysfunction, suppress myocardial inflammation and fibrosis, and alter cytokine expression in rat autoimmune myocarditis.

BACKGROUND: Myocarditis is a clinically serious disease. Tea catechins have been shown to reduce inflammation; however the effects of catechins on the development of myocarditis have not been well studied. AIMS: To clarify the role of catechins, using an experimental autoimmune myocarditis (EAM) model. METHODS AND RESULTS: Lewis rats were immunized with porcine cardiac myosin to establish EAM. Tea catechins were administered orally from day 0 to day 21 (Group A, n=12), from day 14 to day 21 (Group B, n=8), or saline (Group C, n=9) daily. Rats were killed on day 21. Echocardiograms indicated that Group A showed significantly improved cardiac function compared to Group C. Pathologically, non-treated EAM hearts showed severe myocardial cell infiltration and fibrosis; however Group A showed significantly less area. Immunohistochemistry revealed enhanced expression of NF-kappaB and ICAM-1 in non-treated EAM hearts, which was suppressed by catechin administration in Group A. mRNA levels of TNF-alpha were decreased and Th2 cytokines were markedly enhanced in Group A compared with the control group. Late catechin administration (Group B) showed limited effects on EAM. CONCLUSION: The catechins suppressed ventricular remodelling in EAM; thus catechin treatment might be a promising option for the prevention of EAM myocarditis.

Animals↗
PubMed2005

Mitral valve repair versus replacement for isolated non-ischemic mitral regurgitation in patients with preoperative left ventricular dysfunction. A long-term follow-up echocardiography study.

UNLABELLED: The aim of this study was to evaluate LV function, by means of echocardiography, after mitral valve repair (MVr) or mitral valve replacement (MVR) in patients (pts) with chronic degenerative mitral regurgitation (MR) and depressed LV systolic function during a 6-years follow-up (FU) period. PATIENTS AND METHODS: Forty-five pts with moderately severe or severe MR and preoperative EF<or=50% were divided into 2 groups: MVr group (27 pts, 19 men-8 women, aged 62+/-10 years) and MVR group (18 pts, 8 men-10 women, aged 60+/-12 years). The cause of MR was myxomatous mitral valve disease (MVr/MVR: 16/8), endocarditis (0/4) and degenerative mitral valves with ruptured chordae tendineae (11/6). All pts underwent transthoracic echocardiography preoperatively, postoperatively and annually during the FU period (6+/-3 years). RESULTS: In MVr group, 5 pts died, 5 were lost to FU and 2 pts underwent MVR due to MVr failure. In MVR group, 6 pts died, 3 were lost to FU and 1 was re-operated due to prosthetic valve endocarditis. Atrial fibrillation was similar between the 2 groups. MVr pts demonstrated significant LVEDD decrease postoperatively which was persistent during FU (p<0.05). LVESD also decreased (p<0.05), VTI improved (p<0.05), while FS and EF showed a trend to improve. In MVR pts, LVEDD was decreased (p<0.05) but increased during FU (p<0.05) and LVESD remained high, resulting in a decrease of FS and EF (p<0.05). VTI remained unchanged (p=NS). CONCLUSION: MVr in pts with non-ischemic MR and preoperative LV dysfunction achieves better preservation of LV systolic indices than MVR, probably due to preservation of the subvalvular apparatus and LV geometry.

Aged↗
PubMed2005

Revascularization in severe left ventricular dysfunction: the role of viability testing.

Revascularization is a treatment option for moderate-to-severe ischemic cardiomyopathy. Limitations of the current literature, lack of completed randomized trials, and higher periprocedural risks create significant uncertainty about the optimal treatment strategy. This review focuses on the available literature describing the effect of revascularization on outcome and the role of noninvasive viability testing. It attempts to identify a subset of patients likely to benefit from therapy.

Algorithms↗
PubMed2006

Myocardial glucose transport and utilization in patients with type 2 diabetes mellitus, left ventricular dysfunction, and coronary artery disease.

OBJECTIVES: This research was designed to assess the effect of type 2 diabetes mellitus (T2DM) on myocardial glucose utilization in patients with heart failure secondary to coronary artery disease. BACKGROUND: Patients with T2DM and coronary artery disease have an increased morbidity and mortality compared with patients with coronary artery disease without diabetes that may relate to a reduction in the ability of the myocardium to utilize glucose. METHODS: Myocardial blood flow and glucose utilization were assessed during a hyperinsulinemic clamp by 18F-flurodeoxyglucose and positron emission tomography in 54 patients (19 with T2DM) with multivessel coronary artery disease and heart failure. In a subgroup of 18 patients, myocardial biopsies were obtained during coronary bypass surgery to assess glucose transporter (GLUT4) distribution and protein concentration, and compared with myocardium from transplant donor hearts. RESULTS: Myocardial blood flow was similar in patients without diabetes and those with T2DM. Myocardial glucose utilization was lower in patients with T2DM (0.34 +/- 0.16 vs. 0.47 +/- 0.24 micromol x min(-1) x g(-1), p = 0.0002) despite comparable plasma insulin concentrations and a higher blood glucose concentration. Extraction of glucose by the myocardium was reduced in patients with T2DM (7.1 +/- 3.1% vs. 13.5 +/- 5.2%, p < 0.01). Myocardial GLUT4 protein was similar in patients with and without T2DM (p = 0.75). CONCLUSIONS: Patients with coronary artery disease and heart failure exhibit myocardial insulin resistance, and this is greater in those with T2DM. This may limit the ability of the myocardium in patients with T2DM to withstand ischemia and may contribute to the increased cardiovascular morbidity and mortality in such patients.

Aged↗
PubMedDate not supplied

Novel troponin T mutation in familial dilated cardiomyopathy with gender-dependant severity.

Mutations in sarcomeric proteins can lead to either hypertrophic or dilated cardiomyopathy depending on their effects on the structural and functional properties of the contractile unit of the heart. Mutations in cardiac troponin T, which binds the calcium-responsive troponin complex to alpha-tropomyosin, have been shown to result in cardiac hypertrophy or cardiac dilatation and heart failure, depending on the nature of the specific mutation. In this study, we report the identification of a novel cardiac troponin T mutation (A171S) leading to dilated cardiomyopathy and sudden cardiac death. In contrast to prior described mutations, the A171S mutation results in a significant gender difference in the severity of the observed phenotype with adult males (over 20 years of age) demonstrating more severe ventricular dilatation [left ventricular end diastolic dimension (LVEDD) 7.1 vs. 5.1cm; P=0.01, t test] and left ventricular dysfunction [left ventricular shortening fraction (LVSF) 21 vs. 34%; P=0.04, t test] than adult females. The described mutation substitutes a hydrophilic amino acid for a hydrophobic one in a highly conserved domain involved in the interaction between troponin T and alpha-tropomyosin. Interestingly, four previously described mutations within 12 amino acids of A171 lead to a hypertrophic phenotype, suggesting that further characterization of the functional consequences of the A171S mutation may lead to a better understanding of the pathophysiology of DCM and of the functional differences between HCM- and DCM-causing mutations in cardiac troponin T.

Adult↗
PubMed1997

Beneficial effects of a Ca2+ sensitizer, MCI-154, on the myocardial oxygen consumption-cardiac output relation in patients with left ventricular dysfunction after myocardial infarction: comparison with dobutamine and phosphodiesterase inhibitor.

Although conventional inotropic agents such as catecholamines increase myocardial oxygen consumption, a newly developed inotropic agent, a Ca2+ sensitizer, may be able to increase cardiac output with less myocardial oxygen consumption. By using right-side heart catheterization, we assessed the ratio of the increase in myocardial oxygen consumption per unit increase in cardiac output during beta-adrenergic receptor stimulation (dobutamine, n = 15), phosphodiesterase inhibition (E-1020, n = 10), and Ca2+ sensitization (MCI-154, n = 17) in patients with coronary artery disease. Dobutamine increased cardiac output and myocardial oxygen consumption. E-1020 increased cardiac output but did not change myocardial oxygen consumption. MCI-154 increased cardiac output and decreased myocardial oxygen consumption. The oxygen cost of increasing cardiac output with dobutamine and with E-1020 was different from that with dextran infusion (n = 18); in contrast, the oxygen cost with MCI-154 was significantly smaller. Thus a newly developed Ca2+ sensitizer, MCI-154, may be beneficial for the treatment of heart failure.

Cardiac Output↗
PubMed1998

Evidence of left ventricular dysfunction in children with merosin-deficient congenital muscular dystrophy.

BACKGROUND: Deficiency of the sarcolemmal protein dystrophin has been linked to dilated cardiomyopathy. Some children with congenital muscular dystrophy have a deficiency of the laminin alpha2 chain of merosin, an extracellular matrix protein linked to dystrophin through a group of glycoproteins. It has been shown that deficiency in one of these glycoproteins is responsible for muscular dystrophy and dilated cardiomyopathy. Children with laminin alpha2 deficiency may be at risk for development of cardiomyopathy. METHODS AND RESULTS: We studied the cardiac function of a cohort of 16 children with congenital muscular dystrophy by using 2-dimensional echocardiography. The expression of the laminin alpha2 of merosin in the patients was determined on a skin or muscle biopsy. Two of 6 merosin-deficient children had an ejection fraction <40%. The average ejection fraction of the merosin-deficient children was 43%+/-11%, which was significantly lower than the merosin-positive children (53%+/-5%, P=.03). CONCLUSIONS: This study suggests that a deficiency of laminin alpha2 can give rise to dilated cardiomyopathy, supporting the idea that defects of dystrophin, or of associated proteins, can cause dilated cardiomyopathy in addition to muscular dystrophy.

Adolescent↗
PubMed2001

Impact of presentation of research results on likelihood of prescribing medications to patients with left ventricular dysfunction.

This study was conducted to evaluate willingness to prescribe medication based on identical data presented in different outcome terms to health professionals of varied discipline, geographic location, and level of training. Cross-sectional survey using a self-administered questionnaire was performed in 400 health professionals (physicians, pharmacists, physicians-in-training, and pharmacy students) in the United States and Europe. Data reflecting a clinical trial were presented in 6 outcome terms: 3 terms describing identical mortality (relative risk reduction, absolute risk reduction, and number of patients needed to be treated to prevent 1 death); and 3 distractors (increased life expectancy, decreased hospitalization rate, and decreased cost). Willingness to prescribe and rank order of medication preference assuming willingness to prescribe were measured. The results of the study showed that willingness to prescribe and first choice preference were significantly greater when study results were presented as relative risk reduction than when identical mortality data were presented as absolute risk reduction or number of patients needed to be treated to avoid 1 death (p <0.001). Increase in life expectancy was the most influential distractor. In conclusion, this study, performed in the era of "evidence-based medicine," demonstrates that the method of reporting research trial results has significant influence on health professionals' willingness to prescribe. The high numerical value of relative risk reduction and the concrete and tangible quality of increased life expectancy exert greater influence on health professionals than other standard outcome terms.

Cardiovascular Agents↗