Cardiopulmonary and metabolic responses to maximum exercise and aerobic capacity in hemiplegic patients

This study evaluated cardiopulmonary and metabolic responses to maximum exercise and aerobic capacity in hemiplegic patients and clarified the relationship between the resulting data and motor disability. Twenty patients with stroke and fifteen healthy controls were included in the study. Cardiopulmonary and metabolic responses to maximum exercise were investigated with an electronically braked arm crank ergometer. Vital capacity, forced expiratory volume in 1 second, peak expiratory flow rate, forced vital capacity, maximum voluntary ventilation, peak power output, respiratory exchange ratio, and exercise time were reduced in stroke patients when compared with the controls. No relationship was found between these data and motor disability. The hemiplegic patients showed a significant respiratory dysfunction and reduced exercise tolerance. These findings suggest that a program of ventilatory and aerobic training should be considered early after stroke to avoid cardiorespiratory problems and deconditioning.     

Double-chambered right ventricle mimicking asymmetric septal hypertrophy

Double-chambered right ventricle (DCRV) is an uncommon congenital heart disease. Anomalous muscle bundles in the right ventricle divide the right ventricle into two portions and cause intracavitary obstruction of the right ventricle. We report a patient with DCRV mimicking asymmetric septal hypertrophy. We did clinical, echocardiographic and angiographic evaluation. Surgical intervention was successfully managed.     

Infected myocardial hydatid cyst imitating left ventricular aneurysm

We report a case of infected intracardiac hydatid cyst in a patient who had complaints of chest pain, exertional dyspnea, palpitation, evening fever and fatigue. Echocardiography demonstrated a left ventricular apical cystic mass in 7 cm diameter. Magnetic resonance imaging and hemagglutination test confirmed the diagnosis. Single capsulated cyst full of pus was surgically removed by using cardio-pulmonary bypass. Histopathological examination revealed an infected hydatid cyst. Postoperative recovery was uneventful and the patient remains free of symptoms after one year of follow-up.     

Effect of transvenous cardiac resynchronization therapy device implantation on cardiac troponin I release

BACKGROUND: Pacemaker and implantable cardioverter defibrillator (ICD) implantation increases cardiac troponin I (cTnI) levels which indicates myocardial injury. During implantation of a cardiac resynchronization therapy (CRT) device, balloon inflation for coronary sinus (CS) venogram, cannulation of CS side branch, and electrode advancement may interfere with CS drainage and, hence, may decrease the washout of toxic metabolites from the heart. Thus, CRT implantation may further increase cTnI levels. In this study, we investigated the effects of CRT implantation on cTnI release. METHODS: We included 10 patients (mean age = 57 +/- 15 years) in whom a successful transvenous CRT system was implanted (CRT group). Twenty patients (mean age = 65 +/- 10 years) who underwent a transvenous pacemaker or ICD implantation were included as the control group. Blood samples for cTnI were drawn at baseline and at six, 12, 18, and 24 hours thereafter. RESULTS: Baseline median cTnI levels were similar in CRT and control groups (0.03 ng/mL vs 0.02 ng/mL, respectively; P = 0.1). Postoperative cTnI levels during 24 hours were significantly higher in the CRT group (P < 0.05) by two-way repeated measures of analysis of variance. Post hoc analysis revealed that cTnI levels were higher at the 6th, 12th, 18th, and 24th hours compared to baseline levels (P < 0.001, P < 0.001, P < 0.01, and P < 0.01, respectively). There was a significant difference in the area under the curves (AUCs) of cTnI measurements (1.79 hr.ng/mL in the CRT group and 0.78 hr.ng/mL in the control group, P < 0.05). CONCLUSION: Postoperative cTnI levels were higher after CRT implantation than simple pacemaker/ICD implantation. This may be due to CS manipulation during CRT implantation.     

Aortic and coronary artery dissection during percutaneous coronary intervention: a case report and review article

Coronary artery dissection is an uncommon but potentially serious complication in percutaneous coronary interventions. We treated a 53-year-old female patient with right coronary spasm, which was misdiagnosed as a coronary lesion. The coronary spasm resolved with nitrate administration, but proximal coronary dissection developed during angiography. It progressed anterograde and led to inferior myocardial infarction and severe hemodynamic instability due to right coronary artery occlusion. Percutaneous intervention failed, and it was determined that coronary dissection progressed retrograde, across the truncus of the aorta. Ascending aortic grafting and coronary bypass surgery were performed. The patient recovered and was discharged after 10 days. Close cardiothoracic observation is mandatory in patient evaluation and management.     

Protein tyrosine phosphatase receptor-type O (PTPRO) exhibits characteristics of a candidate tumor suppressor in human lung cancer

Previous study in our laboratory demonstrated suppression of the gene for protein tyrosine phosphatase receptor-type O (PTPRO) in primary and established rat hepatomas. The present study showed methylation-mediated silencing of this gene in primary human lung tumors and in several human lung cancer cell lines, one of the characteristics of many tumor-suppressor genes. The reduced expression of PTPRO in the primary lung tumors correlated with the methylation status of its CpG island. Demethylation of the gene by deoxy-5-azacytidine treatment led to its reactivation in a lung cancer line (A549). Overexpression of PTPRO in A549 cells inhibited anchorage-independent growth, delayed reentry of the cells into the cell cycle after release from cell-cycle arrest, and increased susceptibility of the cells to apoptosis. These data have demonstrated the growth-suppressor characteristics of PTPRO that are unique to a classical tumor suppressor.