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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the pathophysiology of chronic cyanosis, we subjected 14 adult mongrel dogs to diversion of the inferior vena cava to the right inferior pulmonary vein. This produced a mean oxygen tension of 42 +/- 2 mm Hg and a calculated right-to-left shunt of 52.0% +/- 3.9%. These animals (Group C) and 15 normal dogs (Group N) were subjected to cardiopulmonary bypass with 20 minutes of normothermic global ischemia. Functional indices studied were rate of rise of left ventricular pressure and the end-systolic pressure/volume ratio. Metabolic status was assessed by obtaining transmural myocardial biopsy specimens for measurement of adenosine triphosphate content. Myocardial blood flow was measured with radiolabeled microspheres. There were no significant differences between Group C and Group N in either functional index or blood flow measurement prior to global ischemia. At 45 minutes after ischemia, Group N animals had a significantly greater rate of rise of left ventricular pressure (at a left ventricular end-diastolic pressure of 0, 5, 10, and 15 mm Hg, p less than 0.025 to 0.05) and subendocarial perfusion (endocardial/epicardial flow ratio 0.961 +/- 0.037 versus 0.815 +/- 0.021, p less than 0.01). At 90 minutes after ischemia, Group N animals exhibited a significantly higher end-systolic pressure/volume ratio (4.9 +/- 0.7 versus 3.0 +/- 0.4 mm Hg/ml, p less than 0.05), rate of rise of left ventricular pressure (at an end-diastolic pressure of 0 to 20 mm Hg, p less than 0.005 to 0.05), and endocardial/epicardial flow ratio (1.065 +/- 0.046 versus 0.829 +/- 0.059, p less than 0.01). No differences in adenosine triphosphate content were found at any sampling period. The Group C left ventricles exhibited no hypertrophy but were significantly dilated compared to Group N (38.8 +/- 0.3 versus 30.1 +/- 0.2 mm, p less than 0.05). Inferior vena cava to pulmonary vein diversion produces cyanosis with left ventricular dilatation but without hypertrophy. It is proposed that abnormal loading characteristics of the left ventricle are responsible for the functional derangements that result from global ischemia.
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PMID:Pathophysiology of chronic cyanosis in a canine model. Functional and metabolic response to global ischemia. 402 30

Compliance of the infarcted left ventricle was studied in dogs 3-5 days after occlusion of the left anterior descending coronary artery. Compliance was assessed from postmortem pressure-volume curves and from pressure-length measurements (mercury-in-silastic segment length gauges) made both in vivo and postmortem. Postmortem pressure-volume curves showed reduced compliance compared to sham-operated animals. Postmortem pressure-length curves of infarcted and adjacent normal myocardium indicated that the diminished total compliance could be attributed to an increase in stiffness of the infarcted area. This was confirmed by in vivo end-diastolic pressure-length changes produced by transient aortic occlusion. The infarcted area was akinetic, showing neither contraction nor aneurysmal bulging. In addition, anesthetized dogs with infarcts, when compared with sham-operated animals, had similar left ventricular end-diastolic volumes (indicator dilution method), but higher left ventricular end-diastolic pressures. Taken with previous observations, which show that systolic aneurysmal bulging is uniformly present at the onset of ischemia, these results indicate that stiffening of the ischemic myocardium occurs during the first 5 days after infarction, and show that elevation of left ventricular filling pressure does not necessarily signify ventricular dilatation. The results also suggest a mechanism whereby ventricular performance may improve during recovery from acute myocardial infarction.
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PMID:Experimental myocardial infarction. IV. Reduction of left ventricular compliance in the healing phase. 491 78

Since elevation of plasma concentrations of free fatty acids (FFA) increases myocardial oxygen consumption without influencing mechanical performance in normal hearts, it was the purpose of this study to determine whether FFA would modify mechanical performance at limited oxygen supply. Left coronary blood flow was reduced by gradual clamping of a shunt from the left carotid artery until moderate ventricular dilatation supervened. Left ventricular systolic pressure (LVSP), its maximal rate of rise (dP/dt) and stroke volume (SV) were unchanged or slightly reduced. The ischemia resulted in a decrease in myocardial oxygen consumption (MVO(2)) from 9.7+/-1.1 ml/min to 7.9+/-0.8 ml/min, and myocardial lactate uptake was reduced or reversed to excretion. Increasing the plasma concentrations of FFA from 359+/-47 muEq/1 to 3688+/-520 muEq/1 by intravenous infusion of a triglyceride emulsion and heparin resulted in further ventricular dilatation, accompanied by increased excretion of lactate. The ventricular decompensation and enhancement of anaerobic myocardial metabolism associated with increased uptake of FFA was not related to changes in coronary flow, MVO(2), or LVSP. dP/dt and SV were virtually unchanged. Intravenous infusion of glucose/insulin, which lowered plasma concentrations of FFA, reversed ventricular dilatation and lactate excretion. The data support the hypothesis that high concentrations of FFA play a significant role in increasing myocardial oxygen requirement and thereby promote depression of contractility of the hypoxic heart in experimental animals.
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PMID:Effect of free fatty acids on myocardial function and metabolism in the ischemic dog heart. 503 25

The purpose of this study was to evaluate the detectability of stress-induced ischemic lesion in patients with previous myocardial infarction using single photon emission computed tomography (SPECT) producing thallium-201 (T1-201) myocardial perfusion imagings (MPI). Seventy patients underwent stress SPECT by symptom-limited graded bicycle ergometer exercise using a dual-headed rotating gamma camera (Toshiba GCA70A) equipped with a computer system (GMS90). After intravenous administration of 2.5 mCi of T1-201, stress SPECT data at 10 minutes and delayed SPECT data at 3 hours after the injection were collected in the 64 X 64 matrix form covering 360 degrees directions by camera sweep of 180 degrees in 6 minutes, which were immediately followed by conventional planar imagings (PL). Transaxial tomographic image reconstruction was performed by convolution method using a Shepp-Logan's filter. Thereafter, sagittal and coronal tomographic images were reconstructed for about 2 minutes. Image interpretation was assessed visually. The results were as follows: Sensitivity and specificity in detecting the affected vessel with more than 75% stenosis by segmental analysis of myocardial images were higher by SPECT than by PL (LAD 89% and 65%, LCX 68% and 56%, RCA 89% and 76% in sensitivity and LAD 94% and LCX 75%, 92% and 94%, RCA 81% and 59% in specificity, respectively). Sensitivity in detecting both single (82%) and multivessel disease (76%) was fairly high. Detectability of stress-induced ischemia (i.e. occurrence of a new defect in patients with previous myocardial infarction and ST-segment depression in ECG) was significantly higher in SPECT (67%) than in PL (39%, p less than 0.005) and in ECG (39%, p less than 0.005). A perfusion defect in the extensive anterior wall, marked left ventricular dilatation and the widening of the angle toward the apex composed of septal and anterolateral walls in transaxial images were the findings characteristic of anterior myocardial infarction with severe dyskinesis. We conclude that stress SPECT is a useful noninvasive technique for the documentation of the number of vessels affected and severe wall motion abnormality of the LV and for the detection of stress-induced ischemia in previous myocardial infarction.
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PMID:[Detectability of stress-induced ischemic lesion in previous myocardial infarction using 201T1 myocardial single photon emission computed tomography]. 633 58

Recent studies have improved our understanding of the diastolic mechnical properties of intact myocardium. In order to obtain meaningful data, pressures external to the heart should be measured, forces and dimensions should be properly normalized, and measurements should be obtained over a wide range of ventricular volumes. Diastolic filling appears to be a passive phenomenon and is not affected significantly by systolic relaxation or mural inertia. Thus, the relationship between diastolic myocardial force and length is determined primarily by the elastic properties of the muscle and by viscous properties during dynamic filling. In the absence of ischemia, the diastolic mechanics of intact myocardium are not altered significantly by acute physiological interventions. Chronic changes in diastolic properties do occur, however, and are fundamentally important to the regulation of cardiac function. Myocardial creep induced by chronically elevated diastolic presssure produces ventricular dilatation, thereby altering chamber geometry, systolic loading, and overall global function. Thus, a detailed analysis of diastolic mechanical properties is essential to the assessment of the performance characteristics of the intact heart.
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PMID:The diastolic mechanical properties of the intact left ventricle. 644 87

Forty-six neonates with intracranial hemorrhage were classified into three groups on the basis of the major computerized tomography (CT) scan findings: Group I consisted of 24 cases of subarachnoid hemorrhage, Group II 20 cases of intracerebral and/or intraventricular hemorrhage, and Group III two cases of subdural hemorrhage. The initial scans in Group I showed blood in the interhemispheric fissure and the supratentorial recess. Sixty percent had an associated hypodensity in the frontal and/or parietal areas, thought to be an indication of ischemia. Changes in the configuration of the ventricular system were infrequent. Initial scans in Group II showed hematomas as follows: one in the brain stem, five in the basal ganglia, 10 in the temporal lobes, and 11 in the ventricles. In 70% of these cases, changes in the configuration of the ventricular system were seen, including compression of a lateral ventricle by mass effect, ventricular dilatation with blood, and obstructive hydrocephalus. Subarachnoid blood was an associated finding in 55% of cases, and focal and diffuse cerebral edema in 40%. Scans in both Group III patients initially showed a mass effect from a subdural clot. In all, 30 patients had one or more follow-up CT scans, and 13 of these were scanned at regular intervals. None of the Group I patients developed hydrocephalus, but 85% of Group II patients with intraventricular blood extending from an intracerebral hemorrhage had this complication. A seizure disorder occurred in 31% of Group I patients and 20% of Group II patients, where it was seen exclusively in those with an intralobar hematoma. A major motor disturbance occurred in 16% of patients; their Ct scans showed evidence of brain destruction involving enlargement of a lateral ventricle, porencephaly, or focal atrophy. Computerized tomography is a useful adjunct to the diagnosis, management, and follow-up study of neonatal intracranial hemorrhage, and correlates well with the clinical findings.
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PMID:Neonatal intracranial hemorrhage. A clinical and serial computerized tomographic study. 743 Oct 73

Acute PE may lead to right ventricular dilatation and failure. Through ventricular interdependence and decreased left ventricular filling, cardiac output and systemic circulation also may be compromised. The associated decrease in coronary perfusion pressure to the acutely overloaded right ventricle may produce ischemia and worsening right heart failure. This downward cycle of right ventricular failure and ischemia may ultimately progress to right ventricular infarction, circulatory arrest, and death. Certain clinical findings, hemodynamic values, and, particularly, echocardiographic signs can identify right ventricular dysfunction after PE. Detection of right ventricular hypokinesis helps to stratify patients' risk, because right ventricular dysfunction confers a worse prognosis than does normal right ventricular function after PE. The concept of "hemodynamic instability" after PE should be expanded to include right ventricular dilatation and wall motion abnormalities, even among normotensive patients. Aggressive intervention with thrombolytic therapy, vasoactive agents, or mechanical embolectomy may improve right ventricular function and clinical outcome.
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PMID:Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. 748 82

Reduced blood flow produced by bilateral carotid artery occlusion (BCAO) caused multiple histopathological alterations in the cerebral cortex of developing cats. BCAO was performed in the second postnatal week. At 1 and 2 months, global structural observations were made using magnetic resonance imaging (MRI). At 3 months, neuron and glial density, extent of myelination, blood vessel distribution, and the distribution of visual callosal projecting neurons (as visualized with the retrogradely transported tracer horseradish peroxidase) were assessed by light microscopy. MRI showed lateral ventricular dilatation at 1 month in five of eight subjects, with wide-ranging severity, although at 2 months only two animals still had enlarged ventricles. Histological observations at 3 months showed that neuron density in the motor cortex, but not the occipital cortex, of BACO animals was significantly lower than that in controls. BCAO animals had more dilated small vessels, again more evident in the motor cortex than in the occipital cortex. From frontal to occipital cortex, the corpus callosum was thinned and the subcortical white matter was reduced. Even with the reduction of white matter, the number of neurons in visual areas 17 and 18 contributing a callosal projection was much higher than normal. BCAO thus altered cerebral vascularization, caused neuronal death, and reduced myelinization over an area much greater than the direct area of carotid perfusion. The excess callosal projection in these animals suggests that neonatal ischemia interferes with the normal process of axon retraction during development.
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PMID:Consequences of reduced cerebral blood flow in brain development. I. Gross morphology, histology, and callosal connectivity. 750 62

Myocardial dysfunction and silent myocardial ischemia have been identified as important prognostic factors following acute myocardial infarction, also in low risk patients. In postinfarction patients, impaired left ventricular function is the result of fixed scar and reversible contractile dysfunction of viable stunning or hibernating myocardium. Post-extrasystolic potentiation (PESP) during 2-dimensional echocardiographic monitoring may be used to detect the presence of viable myocardium in asynergic myocardial segments. Incidence of reversible contractile dysfunction is a very common phenomenon at predischarge examination after myocardial infarction in asymptomatic patients, and it is independent on the persistence of silent ischemia. A progressive loss of myocardial viability occurs over the first year following the acute phase despite the maintenance of an asymptomatic clinical status. This phenomenon is associated with significant dilatation of the left ventricle. Moreover, silent ischemia is strongly related with this progressive loss of myocardial viability and left ventricular dilatation. Thus, it becomes evident that the most important role of medical and interventional approaches consists of limiting the acute necrosis by reperfusion and in preventing the loss of viable chronically hypoperfused myocardium that appears to be a major factor of left ventricular remodeling and changes over time of prognostication in individual patients. Finally, the presence of viable myocardium by PESP in the arterial zone at risk is highly predictive of 4-year mortality, particularly in patients with low ejection fraction (< 40%), and identifies patients who are suitable candidates for revascularization after myocardial infarction.
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PMID:Reversible contractile dysfunction of viable myocardium. Implications for decision making process in post-infarction patients. 795 36

To clarify the mechanism of initiation and progression of right ventricular myocardial infarction, 35 cases were examined among 236 cases of consecutively autopsied hearts. Twenty-six (52%) of 50 cases with posterior left ventricular infarction showed right ventricular infarction, and no statistical differences were observed in the age, gender, and number of impaired vessels among patients with and without right ventricular infarction. However, more proximal occlusion or more extensive thrombi in the right coronary artery did play a very important role in the genesis of the infarction and its progression. Right ventricular dilatation was frequently associated, probably resulted from the functional disorder of contraction and relaxation of the myocardium. Unusual asynchronous ischemia was observed in the right ventricle concomitantly with posterior left ventricular infarction, suggesting the presence of a protective mechanism against ischemia by the abundant collateral circulation of the right ventricle. In conclusion, right ventricular infarction occurs only with the cease of collateral circulation due to proximal occlusion and the presence of long thrombi in the right coronary artery.
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PMID:[Clinico-pathological study of the mechanism of initiation and progression of right ventricular infarction]. 816 34


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