Home About us Contact
|
Home About us Contact | ||
|
|
||
Right-sided Heart Failure (right-sided + heart_failure)
Selected AbstractsThe Surgical Option in the Management of Acute Pulmonary EmbolismJOURNAL OF CARDIAC SURGERY, Issue 6 2008Justo Rafael Sádaba F.R.C.S. (C/Th) Traditionally this condition has been treated with thrombolysis or anticoagulation and support measures. Surgical embolectomy is carried out in situations of hemodynamic instability or contraindication for thrombolysis. We present our results of surgical embolectomy in patients with massive and submassive PE. Methods: Over a three-year period, we have carried out 20 surgical embolectomies for acute PE. The mean age was 66 years, and there were 11 males. In all cases, the diagnosis had been made by a computerized tomography (CT) pulmonary artery angiography. Nine patients (45%) arrived to the operating theater on inotropes, and two of them (10%) with ventilatory support. All patients underwent a median sternotomy, bicaval cannulation for institution of cardiopulmonary bypass (CPB), and main pulmonary arteriotomy for the removal of the thrombus. Results: The mean bypass time was 45 minutes. Two patients (12%) died after being unable to wean off CPB due to right heart failure. Among the 15 survivors, the median ventilation time in the intensive care unit was 24 hours. Twelve patients (60%) required inotropic support postoperatively for right heart failure. All but one survivor (94%) underwent an insertion of a permanent inferior vena cava filter and were anticoagulated with coumarin. The mean follow-up is 9.8 months and is 100% complete, with a survival of 94.5%. All patients were in the World Health Organization (WHO) functional class I, with no re-admissions for respiratory failure. Conclusion: In patients with acute massive or submassive PE, surgical embolectomy offers a valid therapeutic strategy. A right-sided heart failure is the main complication of this condition. [source] Pacing in Right Ventricular Dysplasia after Disconnection SurgeryJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2000CHUEN TANG M.B.B.S. Pacing in Right Ventricular Dysplasia. This report describes a 33-year-old patient with arrhythmogenic right ventricular (RV) dysplasia who had a dual chamber pacemaker implanted at age 23 years for drug-induced bradycardia. Pacing was continued after right ventricular free-wall disconnection (RVFVVD) at age 24 years. Her pacemaker was not replaced after battery depletion 7 years later. She presented the following year in severe right-sided heart failure. Her old pacemaker generator was replaced. This was followed by rapid resolution of her clinical failure and return to a full, active, physical lifestyle. This observation suggests the potential benefit of dual chamber pacing in patients with RV dysplasia after RVFWD. [source] Congestive heart failure caused by intracardiac tumours in two dogsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 8 2006S. M. Warman Congestive heart failure is a common presentation in small animal practice. Cardiac tumours are an unusual cause of congestive heart failure and, when they occur, usually cause clinical signs associated with pericardial effusion and cardiac tamponade. This case report outlines the clinical and histological findings in two dogs presented with clinical signs of congestive heart failure caused by obstruction of blood flow by intracavitary cardiac tumours. Case 1 showed signs of left-sided heart failure caused by osteosarcoma within the left atrial lumen, and case 2 presented with clinical signs of right-sided heart failure due to haemangiosarcoma occupying the right atrial and ventricular lumens. This case report provides further evidence for the inclusion of intracardiac neoplasia in the differential diagnosis for dogs with clinical signs of congestive heart failure. [source] Serum Cardiac Troponin I Concentration in Dogs with Precapillary and Postcapillary Pulmonary HypertensionJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010C. Guglielmini Background: Pulmonary hypertension (PH) is a disease condition leading to right-sided cardiac hypertrophy and, eventually, right-sided heart failure. Cardiac troponin I (cTnI) is a circulating biomarker of cardiac damage. Hypothesis: Myocardial damage can occur in dogs with precapillary and postcapillary PH. Animals: One hundred and thirty-three dogs were examined: 26 healthy controls, 42 dogs with mitral valve disease (MVD) without PH, 48 dogs with pulmonary hypertension associated with mitral valve disease (PH-MVD), and 17 dogs with precapillary PH. Methods: Prospective, observational study. Serum cTnI concentration was measured with a commercially available immunoassay and results were compared between groups. Results: Median cTnI was 0.10 ng/mL (range 0.10,0.17 ng/mL) in healthy dogs. Compared with the healthy population, median serum cTnI concentration was increased in dogs with precapillary PH (0.25 ng/mL; range 0.10,1.9 ng/mL; P < .001) and in dogs with PH-MVD (0.21 ng/mL; range 0.10,2.10 ng/mL; P < .001). Median serum cTnI concentration of dogs with MVD (0.12 ng/mL; range 0.10,1.00 ng/mL) was not significantly different compared with control group and dogs with PH-MVD. In dogs with MVD and PH-MVD, only the subgroup with decompensated PH-MVD had significantly higher cTnI concentration compared with dogs with compensated MVD and PH-MVD. Serum cTnI concentration showed significant modest positive correlations with the calculated pulmonary artery systolic pressure in dogs with PH and some echocardiographic indices in dogs with MVD and PH-MVD. Conclusions and Clinical Importance: Serum cTnI is high in dogs with either precapillary and postcapillary PH. Myocardial damage in dogs with postcapillary PH is likely the consequence of increased severity of MVD. [source] Assessment of a New Experimental Model of Isolated Right Ventricular FailureARTIFICIAL ORGANS, Issue 3 2009Petronio G. Thomaz Abstract We assessed a new experimental model of isolated right ventricular (RV) failure, achieved by means of intramyocardial injection of ethanol. RV dysfunction was induced in 13 mongrel dogs via multiple injections of 96% ethanol (total dose 1 mL/kg), all over the inlet and trabecular RV free walls. Hemodynamic and metabolic parameters were evaluated at baseline, after ethanol injection, and on the 14th postoperative day (POD). Echocardiographic parameters were evaluated at baseline, on the sixth POD, and on the 13th POD. The animals were then euthanized for histopathological analysis of the hearts. There was a 15.4% mortality rate. We noticed a decrease in pulmonary blood flow right after RV failure (P = 0.0018), as well as during reoperation on the 14th POD (P = 0.002). The induced RV dysfunction caused an increase in venous lactate levels immediately after ethanol injection and on the 14th POD (P < 0.0003). The echocardiogram revealed a decrease in the RV ejection fraction on the sixth and 13th PODs (P = 0.0001). There was an increased RV end-diastolic volume on the sixth (P = 0.0001) and 13th PODs (P = 0.0084). The right ventricle showed a 74% ± 0.06% transmural infarction area, with necrotic lesions aged 14 days. Intramyocardial ethanol injection has allowed the creation of a reproducible and inexpensive model of RV failure. The hemodynamic, metabolic, and echocardiographic parameters assessed at different protocol times are compatible with severe RV failure. This model may be useful in understanding the pathophysiology of isolated right-sided heart failure, as well as in the assessment of ventricular assist devices. [source] | ||||||||||