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

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium-99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The maximum increase in end-diastolic volume was slightly greater in painful than in painless episodes, 38 +/- 8.0% versus 28 +/- 12.4%, but no significant difference was observed in the rate of volume change or in the maximum increase of end-systolic volume (133 +/- 50% and 110 +/- 27.3%), stroke volume (-28 +/- 15% and -25 +/- 12.4%), or ejection fraction (-32 +/- 8.7% and -26 +/- 6.0%). Although the maximum end-diastolic volume achieved is greater in painful episodes, this effect cannot be separated from that of duration, and, furthermore, there was no significant difference in end-diastolic volume at the moment chest pain began. Thus, in patients with angina at rest, transient asymptomatic ST segment shifts are consistently associated with large changes in left ventricular volume, similar to those observed during painful episodes. The rate and extent of acute left ventricular dilatation do not appear to be factors directly causing anginal pain.
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PMID:Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia. 339 67

Dilated cardiomyopathy is a moderately common syndrome resulting from many causes, many of which are yet to be defined. The syndrome is relatively easy to diagnose in its late congestive stage if valvular abnormality, hypertensive disease, and gross myocardial infarction are absent. However, it should be suspected in patients with undiagnosed chest pain, in patients whose severe arrhythmia has no obvious cause, and in any patient with demonstrable ventricular dilatation or systolic malfunction. It may follow infections, especially viral ones and is found in many deficiency diseases, especially diabetes. Repeated episodes of angina due to epicardial disease may result in myocardial "stunning" with ultimate dilation and failure. Microvascular spasm or occlusion may be etiologically important. Dilated cardiomyopathy may be a manifestation of toxins, with ethanol being the most important. Immune mechanisms may play a major role, either independently or in connection with other factors. Early diagnosis may be made with the help of echocardiography, radionuclide angiography, and even coronary arteriography. Gallium scan may be helpful, and if positive myocardial biopsy is indicated. Therapy includes classic measures for congestive failure if it is present: cardiac glycosides, diuretics, antiarrhythmics, and anticoagulants. There is evidence that vasodilators, calcium channel blockers, and beta-adrenergic blockers may be helpful for both general and specific reasons, but these should be used with care. Prednisone and azathioprine may help if there is an inflammatory component. Cardiac replacement remains an ultimate measure.
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PMID:Dilated cardiomyopathy: current concepts. 372 Feb 70

A 19-year-old woman with patent ductus arteriosus and increasingly severe chest pain received various examinations including exercise stress radionuclide test, which revealed hypokinesis and decreased myocardial perfusion in the apex and left ventricular dilatation. Conventional selective coronary arteriography and newly-developed ECG synchronized digital subtraction angiography (DSA) were performed to identify the genesis of her myocardial ischemia. Selective coronary arteriography revealed congenital coronary arterial fistulae in the right and left coronary arteries. The largest fistula was observed around the obtuse marginal artery terminating in the left ventricle. Although stenosis of the left circumflex and left anterior descending arteries (LAD) were not observed, the LAD appeared to be hypoplastic. Hypoplasia of the LAD and the steal phenomenon by arterial fistula could have been responsible for the myocardial ischemia in the apex, but this method did not clearly reveal the area and the degree of myocardial ischemia in the apex. Sequentially subtracted images during the arterial and capillary phases were obtained by utilizing ECG-synchronized DSA for selective coronary arteriography. For these images, densitometric analysis was adapted to the myocardial region, i.e. circumferential densitometry using 21 segments around the left ventricular wall. Decreased myocardial perfusion was clearly demonstrated in the apex in capillary phase images. Moreover, circumferential analysis provided detailed information about the area and the degree of impaired peripheral circulation in the myocardium. This analysis by DSA may prove useful for evaluating myocardial perfusion abnormalities.
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PMID:[Regional myocardial perfusion abnormality detected by digital subtraction angiography in a case of patent ductus arteriosus with coronary arterial fistulae]. 390 94

To contribute for making early diagnosis and treatment of acute pulmonary embolism (APE), we investigated on clinical pictures of 225 patients with APE. Common underlying factors were heart disease, prolonged bed rest, post-surgical state, thrombophlebitis, malignant tumor and post-catheterization state in this order. Dyspnea, chest pain, tachycardia and shock were frequently seen as initial symptoms and signs. Blood screening showed leukocytosis, hypoxemia, hypocapnia and elevated serum LDH. Electrocardiographic findings highly demonstrated were ST.T abnormalities, such as T inversion with ST elevation in V1-3, ST depression in V4-6 and sinus tachycardia. Chest X-rays showed diminished pulmonary vascular marking and pulmonary artery dilation. Right ventricular dilatation were frequently seen on 2-dimensional echocardiograms. Pulmonary artery pressure were elevated up to 49/20 (30) mmHg. Twenty-five percent of the patients died, and the recurrence was seen in 4%. Thus, as soon as APE is suspected by above clinical findings, definitive diagnosis should be obtained by the lung perfusion scan and pulmonary arteriography, then oxygen and thrombolytic agents should be given immediately to prevent the fatal outcome.
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PMID:[Early diagnosis and management of acute pulmonary embolism: clinical evaluation those of 225 cases]. 835 37

The predominant venodilator properties of the nitrates and their augmentation of collateral coronary blood flow to the ischemic myocardium endows them with some ideal characteristics for treating myocardial ischemic syndromes. Additional efficacy stems from the ability of the nitrates to replenish the deficient endothelium-derived relaxing factor (EDRF), nitric oxide (NO), in patients with coronary heart disease and also to inhibit platelet aggregation. In stable angina pectoris, the antianginal and antiischemic effects of oral nitrates are well established. Continuous administration of nitrates may lead to tolerance of their clinical efficacy. Recent studies, however, have demonstrated that when used in recommended doses, tolerance can be avoided during long-term treatment with oral nitrates without provocation of anginal attacks during periods of low nitrate levels at night and early hours of the morning. Thus, prolonged treatment with an asymmetric twice-daily regimen of immediate-release isosorbide-5-mononitrate in patients with stable angina pectoris does not give rise to clinical tolerance, prolongs exercise duration, and delays the onset of myocardial ischemia. In unstable angina pectoris, nitrates rapidly relieve chest pain and ameliorate the electrocardiographic signs of myocardial ischemia. In patients with acute myocardial infarction, early treatment with nitrates prevents left ventricular dilatation, improves pumping function, and reduces the risk of ventricular arrhythmias. In patients with chronic heart failure, oral nitrates improve exercise tolerance and, when given in combination with the systemic arterial dilator hydralazine, extend survival. Meta-analysis of published studies has demonstrated that both intravenous and oral nitrates reduced infarct size and morbidity and mortality in patients with acute myocardial infarction. In the ISIS 4 post-infarction study, isosorbide-5-mononitrate 60 mg once daily was not superior to placebo in reducing mortality risk. However, in the GISSI 3 study, the combination of nitrates with an angiotensin-converting enzyme (ACE) inhibitor reduced mortality risks by 17% in patients with acute myocardial infarction. In both the ISIS 4 and GISSI 3 studies, 62% and 57% of the patients in the placebo and control groups, respectively, were treated with nitrates for control of rest angina, myocardial ischemia, and or left ventricular failure symptoms, and this widespread use of open-label nitrates in the control groups may have diluted the true beneficial effects of nitrates in both studies. Taken together, these many studies with oral nitrate treatment in coronary heart disease and heart failure clearly emphasize that these drugs are safe and play more than a symptomatic role in the management of patients with acute and chronic ischemic syndromes due to coronary artery disease.
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PMID:Oral nitrates: more than symptomatic therapy in coronary artery disease? 921 Oct 13

Electrocardiographic (ECG) findings of pulmonary embolism (PE) include S1Q3T3 pattern, right bundle-branch block, right-axis deviation, and T-wave inversion in medial precordial leads. We report other uncommon ECG changes associated with various symptoms during recurrent PE as documented by computed tomography (CT) scans in a single patients. An 83-year-old woman was admitted with PE secondary to deep venous thrombosis in the left leg. During episodes of chest pain, ECG showed QTc prolongation (480 ms) with new T-wave inversion in leads III, aVF, and V1-V3, and ST-segment depression in leads V5-V6. Despite adequate anticoagulant therapy, recurrent episodes of PE occurred in the hospital. When the patient experienced sudden chest tightness, ECG showed a new S-wave notch in lead V1 and clock-wise rotation with sinus tachycardia. She also experienced transient syncope with hypotension. At this time, ECG showed transient atrioventricular junctional rhythm followed by sinus arrest, and CT scan showed a new massive embolus in the main pulmonary trunk with right ventricular dilatation, as demonstrated by echocardiography. The mechanism responsible for QTc prolongation with ST-T changes, the S-wave notch in lead V1 with clockwise rotation, or atrioventricular junctional rhythm with sinus arrest during PE may be associated with myocardial ischemia, acute right ventricular overload, or vagal reflex, respectively.
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PMID:Uncommon electrocardiographic changes corresponding to symptoms during recurrent pulmonary embolism as documented by computed tomography scans. 982 4

A 58-year-old woman with a previous anterior myocardial infarction, recurrent chest pain, transient adenosine-induced left ventricular dilatation but no apparent epicardial disease on angiography is presented. Transient ischemic dilatation during myocardial perfusion imaging, and the reported causes of transient left ventricular dilatation in the absence of epicardial disease, are discussed.
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PMID:Transient left ventricular dilatation in the absence of epicardial disease on angiography. 1516 80

A rare case of primary pulmonary hypertension was observed in a 73-year-old man. Angina pectoris was diagnosed at the age of 67 and he received several percutaneous coronary interventions because of refractory restenosis. He also had coronary artery bypass surgery at the age of 69. After 4 years, he again suffered from dyspnea and chest pain upon physical exertion. On admission to our hospital, a chest radiograph showed dilatation of bilateral pulmonary arteries. Moreover, echocardiography showed right ventricular dilatation and tricuspid regurgitation. Continuous wave Doppler imaging revealed a pressure gradient of 82.1 mmHg. Pulmonary capillary wedge pressure was normal, but pulmonary artery pressure was elevated upon cardiac catheterization. Because there was no apparent etiology of pulmonary hypertension, primary pulmonary hypertension was diagnosed and appropriate conventional therapy was started.
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PMID:[A 73-year-old man with primary pulmonary hypertension]. 1573 71

Still's disease is a subset of juvenile idiopathic arthritis (JIA) that usually presents with intermittent fever, rash, and arthritis. Extra-articular flares can occur several years after disease onset. We report two cases of adult Still's disease with myocarditis after several years of being in remission. A 34-year-old Caucasian man with history of systemic juvenile arthritis in remission since age 13 was admitted in hospital with 10 days history of fever, odynophagia, and arthralgias. Chest X-ray and cardiac ultrasound showed cardiac enlargement. An endomyocardial biopsy revealed acute myocarditis. He was treated with methylprednisolone and intravenous gammaglobulin, with improvement of his general condition and cardiac parameters. A 16-year-old Caucasian male patient with history of systemic JIA in remission for the last 7 years was admitted with 7 days history of fever, odynophagia, arthralgias, and myalgias. Two days after admission, he developed chest pain and pericardial rubbing was found on examination. Cardiac ultrasound showed left ventricular dilatation with impaired systolic function, and posterior, inferior and apical-septal wall hypokinesia. Blood test showed elevated creatine phosphokinase levels. He was treated with IV methylprednisolone with normal follow-up cardiac ultrasound. Cardiac involvement in patients with systemic JIA can be the first symptom of disease reactivation, even after many years of disease remission.
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PMID:Myocarditis as a form of relapse in two patients with adult Still's disease. 1957 28

Noncompaction of the ventricular myocardium (NVM) is a rare unclassified cardiomyopathy which is characterized by multiple prominent trabeculations and deep intertrabecular recesses. This cardiomyopathy can be isolated or in combination with other congenital cardiac disorders, including coronary artery abnormalities. A 56-year-old female patient presented to the cardiology department with complaints of exertional dyspnoea and chest pain. Transthoracic echocardiography revealed left ventricular dilatation with diffuse hypokinesis. Multiple prominent trabeculations with deep inter-trabecular recesses were observed at the left ventricular apex. Also, coronary angiography demonstrated a sinoatrial node artery originating from the posterolateral branch of the right coronary artery.
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PMID:Left ventricular noncompaction associated with a sinoatrial node artery originating from the posterolateral branch of the right coronary artery. 2144 86


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