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)

Collagen which is present in the myocardium in relatively small amounts is the most abundant structural protein of the connective tissue network. Its structural organization consists of a complex weave of collagen fibers that surrounds and interconnects myocytes, groups of myocytes, muscle fibers and muscle bundles. The conformation of interstitial fibrillar collagen makes it highly resistant to degradation by all proteinases other than specific collagenases. In hearts with myocardial damage secondary to myocardial infarction, chronic ischemia, inflammation, or cardiomyopathy, a complex sequence of compensatory events occur that eventually result in an adverse left ventricular remodeling. This continual state of remodeling is characterized by persistent collagenase activity, fibrillar collagen degradation, and progressive myocyte loss. The net effect is a shift in the balance between collagen synthesis and degradation which leads to an inadequate fibrillar collagen matrix, progressive ventricular dilatation and sphericalization with wall thinning and eventual congestive heart failure.
 ...
PMID:Ventricular remodeling in heart failure: the role of myocardial collagen. 854 Apr 1

Right ventricular cardiac function is altered by abnormalities affecting primarily the left-sided cardiac structures, the lungs, or the right-sided cardiac structures themselves. The most common cardiac causes for right ventricular dysfunction are chronic left ventricular ischemia and rheumatic mitral valvular disease. Pulmonary diseases that result in right ventricular dysfunction include pulmonary air-space disease, including emphysema, and pulmonary interstitial and parenchymal diseases, including idiopathic pulmonary fibrosis and cystic fibrosis. Chronic pulmonary vascular disease, including chronic thromboembolism and PPH have a significant effect on right ventricular performance. Common to all of these diseases is elevation of pulmonary vascular resistance with a commensurate increase in right ventricular pressure, resulting in right ventricular hypertrophy. The limited ability of right ventricular myocardium to function in the face of increased pulmonary resistance results in right ventricular dilatation, tricuspid regurgitation, and ultimately right ventricular failure. MR imaging provides direct, noninvasive visualization of the right ventricular chamber as well as the myocardium itself, allowing reliable demonstration of morphologic changes in the size and shape of the ventricle, thickness of the myocardium, and presence of abnormal infiltration by fat or edema. Furthermore, because MR imaging techniques do not depend upon geometric assumptions about the complex shape of the right ventricle, they may be used for accurate and reproducible quantitation of right ventricular volume and myocardial mass.
 ...
PMID:MR imaging of pulmonary hypertension and right ventricular dysfunction. 872 68

The burden of ischemic heart disease is high in dialysis patients. Ischemia may result from atherosclerotic and nonatherosclerotic disease and may cause myocardial infarction and angina. The impact of diminished perfusion is intricately associated with the underlying cardiomyopathy, both of which predispose to heart failure. The etiology of ischemia is complex and associated with the underlying cardiomyopathy, whether it be concentric left ventricular hypertrophy, left ventricular dilatation, or systolic dysfunction. Hypertension, diabetes, dyslipidemia, abnormalities of divalent ion metabolism, hypoalbuminemia, and left ventricular hypertrophy are probably adverse risk factors for ischemia, but the relative importance of each is unknown.
 ...
PMID:Ischemic heart disease in chronic uremia. 887 58

While evaluating 45 hypertensive patients with left ventricular hypertrophy (LVH) for enrollment in a clinical research protocol, we had the opportunity to compare anatomic and functional characteristics of those with LVH and ischemia on an exercise tolerance test (ETT), but without coronary artery disease by angiography (group I, n=8), versus those with a normal ETT (group II, n=37). There were no differences in age, sex, severity, and duration of hypertension between the two groups, but group I patients were significantly more overweight and had a worse lipid profile. Blood pressure at peak ETT was higher in group I despite shorter exercise duration, although resting and ambulatory pressures were similar. Group I patients had evidence of more pronounced cardiac enlargement and LVH by both ECG and echo criteria and a characteristic pattern of more pronounced thickening at the apex, but both groups had equally good systolic function and similar degrees of mild diastolic dysfunction. Analysis of 24-hour ambulatory ECG showed a significantly greater propensity to ventricular arrhythmias in group I, as shown by the presence of late potentials in 4 patients, the presence of couplets in 3, runs of ventricular tachycardia in 2 (while none of group II patients had late potentials or complex arrhythmias), and an average frequency of isolated premature ventricular contractions approximately three times higher in group I than group II patients. Our data demonstrate that hypertensives with LVH associated with myocardial ischemia at stress but with normal coronary arteriograms tend to be more overweight, attain a higher systolic blood pressure at ETT despite a shorter duration, have a higher propensity for severe arrhythmias, and have an adverse lipid profile. LVH in these subjects is more pronounced by both ECG and echo criteria and is characterized by predominantly apical hypertrophy with left atrial and ventricular dilatation rather than overall LV wall thickening.
 ...
PMID:Hemodynamic and humoral correlates in essential hypertension: relationship between patterns of LVH and myocardial ischemia. 932 14

We describe a patient who presented with acute ischemia affecting the left lower limb. Because a transthoracic echocardiogram was abnormal, a transesophageal study was arranged. This demonstrated an atrial septal aneurysm and right-to-left shunting of contrast, raising the possibility of paradoxical embolism. The diagnosis was confirmed by contrast venography, which showed extensive thrombosis in the deep veins of the left thigh, and a ventilation-perfusion scan which was consistent with multiple pulmonary emboli. Among the lessons from this case was the finding that in patients with arterial embolism the likely origin of the embolus should be considered and, in the absence of common risk factors (atrial fibrillation, rheumatic heart disease, left ventricular dilatation, widespread atheroma), occult venous thrombosis and a right-to-left shunt should be sought. In this select group of patients, transesophageal echocardiography is significantly more sensitive than transthoracic study and should be the investigation of choice. Second, in the patient described in this report the clinical signs of deep venous thrombosis (DVT) were masked by the more prominent features of acute arterial ischemia. Without the incidental echocardiographic abnormality, it is likely that the important diagnoses of DVT, pulmonary embolism, and paradoxical embolism would not have been made.
 ...
PMID:Venous thrombosis causing arterial embolization to the same limb through a patent foramen ovale. 937 29

First-day thallium-201 myocardial perfusion scans and technetium-99m RBC gated scintiangiography were performed during the initial clinical and prognostic evaluation of 69 patients with suspected acute myocardial infarction. Patients were monitored for clinical course, diagnosis confirmation, and use of specialty services (cardiac catheterization, percutaneous balloon angioplasty, and cardiac surgery) during hospitalization. Myocardial infarction, confirmed in 20 patients, was associated with significantly more left ventricular dilatation, lower ejection fractions, lower peak left ventricular filling rates, wall motion abnormalities, and thallium-201 perfusion defects than nonmyocardial infarction patients. Among all patients, left ventricular dilatation carried a relative risk of myocardial infarction of 5.8; low ejection fraction and right ventricular dilatation were strongly associated with myocardial infarction. A logistic model for congestive heart failure included: left ventricular dilation, lower mean left ventricular filling rates and time to peak filling rates, and abnormal thallium-201 lung:heart uptakes. Among nonmyocardial infarction patients, subsequent cardiac catheterization was predicted by the presence of anterior thallium-201 perfusion defects, Killip functional class II-III, and ischemia on ECG. These findings suggest that early detection of myocardial perfusion defects and cardiac dysfunction by radionuclide scans enhances initial evaluation of suspected acute myocardial infarction patients. Additional studies are needed to confirm these findings.
 ...
PMID:Early radionuclide scans for risk assessment in suspected acute myocardial infarction. 943 58

L-Carnitine can affect cardiac function principally by improving fatty acid and/or glucose metabolism, by increasing perfusion due to modulation of the deformability of erythrocytes and/or vasodilatation, and by stabilising mitochondrial and plasma membranes of cardiomyocytes. While short-term administration of L-carnitine in vivo does not increase the muscular and probably also not the cardiac L-carnitine content, it improves the function of perfused rat or pig hearts in the reperfusion phase after ischemia. Long-term administration of L-carnitine increases the cardiac L-carnitine content in mice and has been shown to improve surrogate markers of coronary heart disease such as arrhythmias, nitrate consumption, and left ventricular dilatation and infarct size in patients after myocardial infarction. The only clear indication for L-carnitine in cardiology is to date cardiomyopathy associated with primary L-carnitine deficiency.
 ...
PMID:[Physiologic bases for the use of L-carnitine in cardiology]. 952 39

We investigated the efficiency of analysis by magnetic resonance imaging (MRI) in cases of hemodynamic vertebro-basilar insufficiency (VBI). We enrolled 76 cases of hemodynamic VBI who had visited our clinic in the Department of Otolaryngology, Nara Medical University, from 1994 to 1996. The evaluation of MRI was classified according to the degree of ventricular dilatation, callosal degeneration, and lacunar infarction, and the evaluation of MR angiography (MRA) was classified according to the degree of pathological change of the blood vessels. There was a significant difference in lacunar infarction on the MRI findings between VBI cases and normal controls, and there were also significant differences in side differences in the vertebral artery between VBI cases and peripheral vertigo and normal control patients. We propose an etiology for hemodynamic VBI: a functional cerebral circulation disorder causes ischemia of the basal ganglia and leads to lacunar infarctions; furthermore, the side difference between the two vertebral arteries causes a circulation disorder in the vertebrobasilar system.
 ...
PMID:Magnetic resonance imaging (MRI) test in hemodynamic vertebro-basilar insufficiency. 965 13

The renin-angiotensin system is activated during myocardial ischemia, and local angiotensin II formation occurs in ischemic hearts. At least two angiotensin II receptor subtypes, the AT1 and AT2 receptor, have been identified. The cardiovascular effects of angiotensin II have been largely attributed to activation of AT1 receptors. In ventricular preparations from normal rat and pig hearts, the density of AT1 receptors is higher than that of AT2 receptors, whereas data on the AT receptor subtype density and its distribution in human hearts remain controversial. AT1 receptor blockade increases coronary blood flow during ischemia in dogs and during reperfusion in rats. It also reduces the incidence of ischemia-related arrhythmias in rats and guinea pigs, limits infarct size in pigs, improves functional and metabolic recovery following myocardial ischemia, and attenuates ventricular remodelling post-myocardial infarction in rats. The potential mechanisms responsible for the cardioprotection by AT1 receptor blockade remain to be elucidated in detail, but appear to involve AT2 receptor activation and the subsequent action of bradykinin, prostaglandins, and/or nitric oxide. Patients under treatment with AT1 receptor antagonists for indications such as hypertension and ventricular dilatation after myocardial infarction are likely to have improved prognosis when suffering an acute myocardial infarction.
 ...
PMID:AT1 receptor blockade in experimental myocardial ischemia/reperfusion. 983 69

Low-energy laser irradiation (LELI) has been found to modulate biological processes. The present study investigated the effect of LELI on infarct size after chronic myocardial infarction (MI) and ischemia-reperfusion injury in rats. The left anterior descending (LAD) coronary artery was ligated in 83 rats to create MI or ischemia-reperfusion injury. The hearts of the laser-irradiated (LI) rats received irradiation after LAD coronary artery occlusion and 3 days post-MI. At 14, 21, and 45 days post-LAD coronary artery permanent occlusion, infarct sizes (percentage of left ventricular volume) in the non-laser-irradiated (NLI) rats were 52 +/- 12 (SD), 47 +/- 11, and 34 +/- 7%, respectively, whereas in the LI rats they were significantly lower, being 20 +/- 8, 15 +/- 6, and 10 +/- 4%, respectively. Left ventricular dilatation (LVD) in the chronic infarcted rats was significantly reduced (50-60%) in LI compared with NLI rats. LVD in the ischemia-reperfusion-injured LI rats was significantly reduced to a value that did not differ from intact normal noninfarcted rats. Laser irradiation caused a significant 2.2-fold elevation in the content of inducible heat shock proteins (specifically HSP70i) and 3.1-fold elevation in newly formed blood vessels in the heart compared with NLI rats. It is concluded that LELI caused a profound reduction in infarct size and LVD in the rat heart after chronic MI and caused complete reduction of LVD in ischemic-reperfused heart. This phenomenon may be partially explained by the cardioprotective effect of the HSP70i and enhanced angiogenesis in the myocardium after laser irradiation.
 ...
PMID:Long-term effect of low energy laser irradiation on infarction and reperfusion injury in the rat heart. 1135 8


<< Previous 1 2 3 4 5 6 7 Next >>