Right ventricular pressure and dilation during pressure overload determine dysfunction after pressure overload.
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Volume expansion and inotropic stimulation are used clinically to augment cardiac output during acute right ventricular (RV) pressure overload. We previously showed that a brief period of RV pressure overload causes RV free wall dysfunction that persists after normal loading conditions have been restored. However, the impact of volume expansion and inotropic stimulation on the severity of RV dysfunction after acute pressure overload is unknown. We hypothesized that the severity of RV dysfunction after RV pressure overload would be related to the level of RV free wall systolic stress during RV pressure overload, rather than to the specific interventions used to augment RV function. Chloralose-anesthetized, open-chest pigs were subjected to 1 h of RV pressure overload caused by pulmonary artery constriction, followed by 1 h of recovery after release of pulmonary artery constriction. A wide range of RV free wall systolic stress during RV pressure overload was achieved by either closing or opening the pericardium (to simulate volume expansion) and by administering or not administering dobutamine. The severity of RV free wall dysfunction 1 h after RV pressure overload was strongly and directly correlated with the values of two hemodynamic variables during RV pressure overload: RV free wall area at peak RV systolic pressure (determined by sonomicrometry) and peak RV systolic pressure, two of the major determinants of peak RV free wall systolic stress. Opening or closing the pericardium, and using or not using dobutamine during RV pressure overload, had no independent effects on the severity of RV dysfunction. The findings suggest that the goal of therapeutic intervention during RV pressure overload should be to achieve the required augmentation of cardiac output with the smallest possible increase in RV free wall systolic stress. (+info)
Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease.
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BACKGROUND: Endothelial vasodilator dysfunction is a characteristic feature of patients at risk for coronary atherosclerosis. Therefore, we prospectively investigated whether coronary endothelial dysfunction predicts disease progression and cardiovascular event rates. METHODS AND RESULTS: Coronary vasoreactivity was assessed in 147 patients using the endothelium-dependent dilator acetylcholine, sympathetic activation by cold pressor testing, dilator responses to increased blood flow, and dilation in response to nitroglycerin. Cardiovascular events (cardiovascular death, unstable angina, myocardial infarction, percutaneous transluminal coronary angioplasty, coronary bypass grafting, ischemic stroke, or peripheral artery revascularization) served as outcome variables over a median follow-up period of 7.7 years. Patients suffering from cardiovascular events during follow-up (n=16) had significantly increased vasoconstrictor responses to acetylcholine infusion (P=0. 009) and cold pressor testing (P=0.002), as well as significantly blunted vasodilator responses to increased blood flow (P<0.001) and the intracoronary injection of nitroglycerin (P=0.001). Impaired endothelial and endothelium-independent coronary vasoreactivity were associated with a significantly higher incidence of cardiovascular events by Kaplan-Meier analysis. By multivariate analysis, all tests of coronary vasoreactivity were significant, independent predictors of a poor prognosis, even after adjustment for traditional cardiovascular risk factors or the presence of atherosclerosis itself. CONCLUSIONS: Coronary endothelial vasodilator dysfunction predicts long-term atherosclerotic disease progression and cardiovascular event rates. Thus, the assessment of coronary endothelial vasoreactivity can provide pivotal information as both a diagnostic and prognostic tool in patients at risk for coronary heart disease. (+info)
Oozing type cardiac rupture repaired with percutaneous injection of fibrin-glue into the pericardial space: case report.
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Two patients, a 56-year-old man and an 81-year-old woman who were admitted to hospital because of anteroseptal acute myocardial infarction, were initially treated successfully with direct percutaneous transluminal coronary angioplasty. However, both patients later developed sudden cardiogenic shock due to cardiac tamponade caused by left ventricular free wall rupture (LVFWR). Prompt, life-saving pericardiocentesis was performed, then fibrin-glue was percutaneously injected into the pericardial space. After the procedure, there was no detectable pericardial effusion on echocardiography and the hemodynamic state became stable. The surgical treatment was the standard procedure for LVFWR, but percutaneous fibrin-glue therapy can also be considered for oozing type LVFWR. (+info)
Nonsurgical transthoracic epicardial catheter ablation to treat recurrent ventricular tachycardia occurring late after myocardial infarction.
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OBJECTIVES: We sought to evaluate feasibility, safety and results of transthoracic epicardial catheter ablation in patients with ventricular tachycardia occurring late after an inferior wall myocardial infarction. BACKGROUND: Transthoracic epicardial catheter ablation effectively controls recurrent ventricular tachycardia (VT) in patients with Chagas' disease in whom epicardial circuits predominate. Epicardial circuits also occur in postinfarction VT. METHODS: Fourteen consecutive patients aged 53.6 +/- 14.5 years with postinfarction VT related to the inferior wall were studied. The VT cycle length was 412 +/- 51 ms. Two patients had previously undergone unsuccessful standard endocardial radiofrequency energy (RF) ablation. The VT was incessant in one patient. Left ventricular angiography showed inferior akinesia in 13 patients and an inferior aneurysm in 1 patient. Ablation was performed with a regular steerable catheter placed into the pericardial sac by pericardial puncture. RESULTS: The pericardial space was reached in all patients. Electrophysiologic evidence of an epicardial circuit was present in 7 of 30 VTs. Due to a high stimulation threshold, empirical thermal mapping was the only criterion used to select the site for ablation. Three VTs were interrupted during the first RF pulse. Two pulses were necessary to render it noninducible in 3 patients (1 VT per patient). In the remaining 4 VTs, 3, 3, 4 and 5 RF pulses, respectively, were used. The overall success was 37.14% (95% confidence interval, 11.83% to 62.45%). Patients are asymptomatic for 14 +/- 2 months. CONCLUSIONS: Postinfarction pericardial adherence does not preclude epicardial mapping and ablation to control VT related to an epicardial circuit in postinferior wall myocardial infarction. (+info)
Effects of the renin-angiotensin system on the current I(to) in epicardial and endocardial ventricular myocytes from the canine heart.
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The Ca(2+)-independent portion of transient outward K(+) current (I(to)) exhibits a transmural gradient in ventricle. To investigate control mechanisms for this gradient, we studied canine epicardial and endocardial ventricular myocytes with use of the whole-cell patch-clamp technique. I(to) was larger in amplitude, had a more negative voltage threshold for activation, and had a more negative midpoint of inactivation in epicardium. Recovery from inactivation was >10-fold slower in endocardium. Incubation of epicardial myocytes with angiotensin II for 2 to 52 hours altered I(to) to resemble unincubated endocardium and reduced the amplitude of the phase 1 notch of the action potential. In contrast, incubation of endocardial myocytes with losartan for 2 to 52 hours altered I(to) to resemble unincubated epicardium and induced a phase 1 notch in the action potential. With RNase protection assays, we determined that incubations with angiotensin II or losartan did not alter mRNA levels for either Kv4.3 or Kv1.4; thus, a change in the alpha subunit for I(to) is unlikely to be responsible. To test whether posttranslational modification produced the effects of angiotensin II, we coexpressed Kv4.3 and the angiotensin II type 1a receptor in Xenopus oocytes. Incubation with angiotensin II increased the time constant for recovery from inactivation of the expressed current by 2-fold with an incubation time constant of 3.7 hours. No effect on activation or inactivation voltage dependence was observed. These results demonstrate that the properties of I(to) in endocardium and epicardium are plastic and likely under the tonic-differing influence of the renin-angiotensin system. (+info)
Primary pericardial mesothelioma presenting as constrictive pericarditis: a case report.
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Primary malignant pericardial mesothelioma is a rare tumor and the case reported here presented as constrictive pericarditis. The patient's symptoms progressed day by day despite treatment with digitalis, diuretics and catecholamines. Although a computed tomographic scan of the chest, echocardiography and pericardiocentesis were performed, a preoperative definitive diagnosis could not be obtained. Emergency pericardiectomy and partial resection of the tumor were carried out with the aid of a percutaneous cardiopulmonary supporting system, but the patient died of cardiac failure on postoperative day 3. The tumor appeared to be the biphasic type of diffuse malignant mesothelioma. The prognosis for pericardial mesothelioma is extremely poor due to its late presentation and difficulty in completely removing it surgically and, unfortunately, there still is not a radical therapy for this tumor. (+info)
Pericardial fluid from patients with unstable angina induces vascular endothelial cell apoptosis.
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OBJECTIVES: The purpose of this study was to investigate whether pericardial fluid from patients with unstable angina (UA) would modulate vascular endothelial cell survival. BACKGROUND: Apoptosis of vascular endothelial cells promotes the coagulation process, playing an important role in the formation of coronary arterial thrombi. However, little is known about the mechanisms of vascular endothelial cell death in acute coronary syndrome. We hypothesized that factors inducing apoptosis are produced by the ischemic heart and accumulated in high concentrations in pericardial fluid. METHOD: Pericardial fluid was obtained during coronary artery bypass surgery from patients with UA (group A, n = 8) and those with stable angina (group B, n = 23). A survival assay of F2 cells from a mouse vascular endothelial cell line was performed in the presence of 10% pericardial fluid from each patient. RESULTS: Pericardial fluid levels of vascular endothelial growth factor were significantly higher in group A than in group B, indicating that group A had more ischemic insults than group B. Pericardial fluid from group A, but not from group B, markedly induced F2 cell death (cell survival relative to fetal bovine serum; group A: 33 +/- 26% vs. group B: 91 +/- 22%, p < 0.01). Cell death was associated with internucleosomal DNA fragmentation, a hallmark of apoptosis. Fractionation of pericardial fluid using a Centricon C-100 demonstrated that apoptosis-inducible activities exist in the Centricon C-100 retentates but not in the filtrates. CONCLUSIONS: Factors that induce vascular endothelial cell apoptosis are secreted into the pericardial space from the hearts of patients with UA. These factors are large complexes or unknown new proteins larger than 100 kDa. (+info)
Multisite pacing for prevention of atrial tachyarrhythmias: potential mechanisms.
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OBJECTIVES: To determine the effects of single-, dual-, triple- and quadruple-site atrial pacing on atrial activation and refractoriness in normal canine hearts. BACKGROUND: Multisite pacing has been suggested to be superior to single-site pacing for prevention of atrial tachyarrhythmias. However, the underlying electrophysiological mechanisms are undetermined at the moment, as is the rationale for the selection of pacing locations and the number of pacing sites. METHODS: In 13 normal beagle dogs, an epicardial multielectrode (128 bipoles) and a multiplexer mapping system were used to reconstruct epicardial atrial activation patterns obtained during simultaneous stimulation from up to four electrodes located in the high and low right and left atrium, respectively. For all pacing modes (single-, dual-, triple- and quadruple-site pacing), total activation times and local effective refractory periods at eight randomly selected sites as well as local recovery intervals were determined. In a subgroup of five dogs, total epicardial activation times were also obtained during single-site septal stimulation (septal group). RESULTS: Activation times and local recovery intervals were minimized by triple-site stimulation, whereas a fourth site did not produce further shortening. Septal stimulation produced epicardial activation times comparable to quadruple-site stimulation. Local refractory periods and their dispersion always remained unaffected. Functional conduction blocks apparent during single-site were found to resolve during multisite stimulation. CONCLUSIONS: Multisite pacing can prevent functional conduction blocks by multidirectional excitation and a reduction in total activation time. Triple-site and, possibly, septal pacing modes are expected to be most efficient because both minimize total activation times and maximize the multidirectionality of excitation. In spite of unaffected local refractory periods, the shortening of local recovery intervals might homogenize atrial repolarization and, thus, contribute to the preventive effects of multisite pacing. (+info)