Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and morphologic features of transmural myocardial infarction (associated with insignificant or absent atherosclerosis of the extramural coronary arteries) are described in seven patients with hypertrophic cardiomyopathy. Marked chronic congestive heart failure associated with supraventricular arrhythmias occurred in six of the seven patients, each of whom had no or mild left ventricular outflow tract obstruction under basal conditions. No patient had typical angina pectoris, and only one patient had clinically evident acute myocardial infarction. Infarction may have caused cardiac arrest in one other patient, but was "silent" in the remaining five patients. At necropsy, six of the seven patients had extensive myocardial scarring involving the ventricular septum, left ventricular free wall and one or both left ventricular papillary muscles; in four patients portions of the right ventricular wall were also scarred. Six patients had dilated ventricular cavities, including two who were known to have nondilated ventricular cavities earlier in their clinical course. It is concluded that transmural myocardial infarction in the absence of significant coronary atherosclerosis is a not uncommon finding (prevalence rate 15 percent) in a population of patients who had died from hypertrophic cardiomyopathy. Although transmural infarction is possibly a secondary event, it more likely contributes causally to the clinical deterioration of some patients with hypertrophic cardiomyopathy, leading to ventricular dilatation and progressive fatal cardiac failure.
 ...
PMID:Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. 57 70

Thirty-four cats with primary myocardial disease were studied. The cats were divided into two groups, depending on the clinical, hemodynamic, angiocardiographic, and pathologic findings. Group A consisted of those cats with hypertrophic cardiomyopathy and Group B consisted of those cats with congestive cardiomyopathy. Similarity in the characteristics of cardiomyopathy in the human cat was found. Both Group A and Group B consisted predominantly of mature adult male cats. The most common presenting signs were dyspnea and/or thromboembolism, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (Group A) or without (Group B) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (Group A) or left ventricular dilatation (Group B). Some cats in Group A also had evidence of left ventricular outflow obstruction. The principal pathologic findings in these cats were left atrial dilatation, symmetric hypertrophy or asymmetric septal hypertrophy of the left ventricle (Group A), and dilatation of the four cardiac chambers (Group B). Aortic thromboembolism was commonly observed in both groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat is similar to the two most common forms of cardiomyopathy in the human (hypertrophic cardiomyopathy, with and without obstruction, and congestive cardiomyopathy).
 ...
PMID:Primary myocardial disease in the cat. A model for human cardiomyopathy. 84 11

Deletions and point mutations of mitochondrial DNA (mtDNA) of patients with dilated or hypertrophic cardiomyopathy were analyzed using the polymerase chain reaction and fluorescence-based direct sequencing. The patients included are with hypertrophic cardiomyopathy associated with left ventricular dilatation, a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and a patient with fatal infantile cardiomyopathy. Deletions were frequently seen in mtDNA in patients with dilated cardiomyopathy. The mtDNA was sequenced and the direct repeat at each edge of deletion was identified as (5'-CATCAACAACCG-3') which was located in the ATPase6 gene and in the D-loop region. In a patient with hypertrophic cardiomyopathy associated with left ventricular dilatation, another mutant mtDNA was found not to have directly repeated sequence, and was revealed to jump from nucleotide position 8,992 to position 16,072 of mtDNA resulting in a 7,079 bp deletion. This patient had unique point mutation in the tRNA genes. A G-to-A transition in the tRNA(Cys) gene (nucleotide position 5,821) at the aminoacyl acceptor stem and an A-to-G transition in the tRNA(Thr) gene (nucleotide position 15,951) were identified. In a patient with MELAS, an A-to-G transition in the tRNA(Leu)(UUR) gene (nucleotide position 3,243) was observed. This mutation was located at the 5' end of the dihydrouridine loop of this tRNA molecule, and would disturb its function. In a patient with hypertrophic cardiomyopathy associated with lactic acidosis, mutations of mtDNA should be suspected.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Mitochondrial DNA mutations in cardiomyopathy. 143 21

Five patients with hypertrophic cardiomyopathy developed left-ventricular dilatation and congestive heart failure during an observation period of 16-29 years. In one patient cardiac transplantation had to be performed. The initial predominant symptoms of outflow-tract obstruction and diastolic dysfunction developed into progressive left-ventricular systolic failure. The question of whether this is a well-defined subgroup of patients with hypertrophic cardiomyopathy, or whether hypertrophic cardiomyopathy turns into a phase of left-ventricular dilatation and failure after some years remains to be elucidated by long-term studies.
 ...
PMID:[Course of dilatative hypertrophic cardiomyopathy]. 187 8

The left ventricular blood flow pattern during the isovolumic relaxation period was investigated in 17 patients with apical hypertrophy (mean 54 +/- 8 years) and 30 with asymmetric septal hypertrophy without left ventricular outflow obstruction (mean 54 +/- 14 years). Thirty-five age-matched normal subjects served as controls (mean 51 +/- 10 years). All cases were examined by pulsed Doppler echocardiography simultaneously with phonocardiography. In all the control subjects, an apically-directed flow was observed, which occurred simultaneously with the onset of the second heart sound. In contrast, a basally-directed flow was detected during the isovolumic relaxation period in 13 patients (76%) with apical hypertrophy and in 28 (93%) with asymmetric septal hypertrophy. In these cases, an apically-directed flow was often observed before the second heart sound. Standard M-mode echocardiography revealed a significant increase in the left ventricular short-axis dimension at the base during the isovolumic period in patients with hypertrophic cardiomyopathy, while the normal controls showed no significant change. Moreover, peak velocity of the basally-directed flow correlated significantly with the rapidity of dilatation of the basal dimension (r = 0.61, p less than 0.01). Thus, this basally-directed blood flow in the left ventricle during the isovolumic relaxation period may be caused by the asynchronous left ventricular dilatation during the isovolumic period.
 ...
PMID:[Paradoxical left ventricular blood flow during the isovolumic relaxation period in non-obstructive hypertrophic cardiomyopathy: Doppler and M-mode echocardiographic study]. 209 64

We performed cardiac catheterisation in a man who had been diagnosed as having hypertrophic cardiomyopathy 7 years earlier. The repeat angiogram showed the maintenance of a "supernormal" systolic function (ejection fraction: 87%) although there was an increase of left ventricular end-diastolic volume (from 65 to 132 ml/m2). This case suggests that progressive left ventricular dilatation should not necessarily be considered a marker of the progression of hypertrophic cardiomyopathy into a hypokinetic left ventricle.
 ...
PMID:The progression of hypertrophic cardiomyopathy: dilatation of the left ventricle with supernormal systolic function. 213 33

Abnormalities in the diastolic function of the left ventricular pump are the common determinant and, above all, the earliest manifestation of all forms of chronic left ventricular failure, whether or not the left ventricular systolic function is abnormal. Congestive signs, in particular, are directly related to abnormalities of ventricular filling. Primary diastolic dysfunction is the cause of left ventricular failure in about 40 p. 100 of the cases, but it may also be observed in almost all cardiopathies. In myocardial ischaemia the pressure-volume relation is displaced upwards owing to a slowed down, inhomogeneous and incomplete relaxation. Left ventricular hypertrophy, whether it is due to excessive pressure (arterial hypertension, aortic stenosis) or reflects a primary hypertrophic cardiomyopathy, is associated with a slowing down of ventricular relaxation and a reduction of left ventricular diastolic distensibility, even though the ventricular pump systolic function remains normal for a long time. Outside alterations in the distensibility of the ventricular muscle, ventricular dilatation alters ventricular filling by forcing the ventricle to function on the vertical part of its diastolic pressure-volume relation. Nowadays, the aged hearts is the most frequent cause of heart failure with normal systolic function. In all cases dysrhythmias and atrioventricular desynchronization act as aggravating factors. Treatment is often difficult since positively inotropic drugs or arterial vasodilators frequently have a modest or even deleterious effect.
 ...
PMID:[Disorders of diastolic function in chronic left ventricular insufficiency]. 214 34

A long-term follow-up (9 years) in a patient with hypertrophic cardiomyopathy revealed an evolution to a hypokinetic and dilated left ventricle. The patient underwent heart transplantation, and therefore the native heart was available for morphologic studies. Gross and microscopic stigmata of hypertrophic cardiomyopathy were present, as well as evidence of left ventricular dilatation. Multiple myocardial scars in both ventricles indicated past ischemic episodes, most probably due to coronary embolization from left ventricular mural thrombi. Other possible pathogenetic mechanisms for the progression of hypertrophic cardiomyopathy to a dilated one are discussed.
 ...
PMID:Hypertrophic cardiomyopathy evolving into a hypokinetic and dilated left ventricle: coronary embolization as a probable pathogenetic mechanism. 236 85

The incidence of hypertrophic cardiomyopathy progressing to dilated cardiomyopathy is rare. A patient diagnosed at age 22 and followed for 24 years who progressed to a dilated cardiomyopathy with severe congestive heart failure is reported. Left ventricular dilatation in hypertrophic cardiomyopathy may be due to a complication of surgery, beta-blocker therapy, or myocardial infarction. It may also represent the natural history in a subset of patients with hypertrophic cardiomyopathy.
 ...
PMID:Progression from hypertrophic cardiomyopathy to dilated cardiomyopathy. 239 73

We investigated the natural course of 59 patients with hypertrophic cardiomyopathy (HCM) in follow-up periods of one to 13 years and analyzed the clinical, hemodynamic and echocardiographic parameters to determine the factors influencing the prognosis. Among these patients, 44 (75%) remained stable in a compensated condition with or without medications. Five patients died suddenly and two died of congestive heart failure. Heart failure developed in another eight. At the initial evaluation, these 15 patients had high left ventricular end-diastolic pressure (mean: 22 +/- 8 mmHg) significantly higher than that of 44 compensated patients (mean: 13 +/- 6 mmHg, p less than 0.001). There were no differences in age at the initial evaluation between compensated and end stage groups. Atrial fibrillation occurred persistently in three and transiently in two among ten patients with heart failure during follow-up periods. Ventricular dimensions and systolic function did not statistically differ between the two groups. However, six patients with heart failure had cavity dilatation and deteriolated ventricular contractile function at the initial evaluation. Four of them did not show any change in left ventricular hypertrophy, but the regional thinning of the wall was observed in the remaining two. There were no characteristic features to predict sudden death in the clinical, hemodynamic or echocardiographic parameters. Thus, increased left ventricular end-diastolic pressure, atrial fibrillation, left ventricular dilatation and the regional thinning of the left ventricular wall are useful predictive markers for poor prognosis in HCM.
 ...
PMID:[Natural course of hypertrophic cardiomyopathy: clinical, hemodynamic and echocardiographic features in the end stage]. 297 74


1 2 3 4 Next >>