Search PubMed⌕ Search

Biomedical subjects

Juan A Crestanello

Publications and source records attributed to Juan A Crestanello.

8 recordsLinked to original sources
PubMed2004

Mitral and tricuspid valve repair in patients with previous mediastinal radiation therapy.

BACKGROUND: The purpose of this study was to evaluate outcomes of mitral and tricuspid valve repair after mediastinal radiation therapy. METHODS: From 1976 to 2001, 22 patients (mean age 61 +/- 14 years) underwent mitral (n = 14), tricuspid (n = 6), or both (n = 2) valve repairs 15 +/- 9 years after mediastinal radiation therapy. Concomitant procedures included coronary artery bypass graft, 11 patients; valve replacement, 6 patients (4 aortic, 3 mitral, 1 tricuspid, and 1 pulmonary); and pericardiectomy, 4 patients. RESULTS: Total follow-up was 82.5 patient-years (mean 3.7 +/- 3.3 years). Early mortality was 3 patients. There were 7 late deaths, 4 of which were of cardiovascular origin. Of the 19 early survivors, 2 required subsequent valve replacements, and 1 required cardiac transplantation 3.4 +/- 2.8 years after valve repair. One patient died after reoperation. In 4 patients who did not undergo reoperation, echocardiographic examinations showed progressive deterioration of their repaired valve function. Overall survival, freedom from cardiac death, and freedom from valve reoperation or cardiac transplantation at 5 years for early survivors was 66%, 85%, and 88%, respectively. New York Heart Association functional class at follow-up was I or II in 8 of the 12 late survivors. CONCLUSIONS: Functional status was good in two-thirds of late survivors. However, severe dysfunction of the repaired valve developed in 32% of early survivors and 16% required further surgery. Valve repair is technically feasible in selected patients after mediastinal radiation therapy; however, the limited durability of repairs after mediastinal radiation in this series suggests that valve replacement might be preferable.

Adult↗
PubMed2004

Thoracic surgical operations in patients enrolled in a computed tomographic screening trial.

OBJECTIVE: Screening for lung cancer with computed tomography may detect cancers at an earlier stage but may also result in overdiagnosis. We reviewed the thoracic surgical operations performed on patients enrolled in our computed tomographic screening program. METHODS: From January 1999 through December 2002, screening computed tomography for lung cancer was performed annually on 1520 participants. All participants were at least 50 years old and smoked more than 20 pack/y. We found 3130 indeterminate pulmonary nodules in 1112 participants (73%). Fifty-five participants (3.6%) underwent 60 thoracic operations for a variety of indications. The medical records of these 55 patients were reviewed. RESULTS: Indications for operation included suspicious pulmonary nodules, mediastinal adenopathy, and a spontaneous pneumothorax. Operations performed included a lobectomy in 37 cases, wedge resection in 11, segmentectomy in 6, video-assisted thoracoscopic surgical talc pleurodesis in 1, bilobectomy in 2, mediastinoscopy in 2, and anterior mediastinotomy in 1. Benign disease was found in 10 patients (18.1%), and lung cancer was found in 45 (81.9%), 2 of whom had metachronous lung cancers. Cell types were adenocarcinoma in 15 cancers, bronchioloalveolar cell carcinoma in 13, squamous cell in 13, carcinoid in 2, small cell in 2, and large cell and undifferentiated non-small cell in 1 case each. Twenty-eight cancers were classified as stage IA, 4 as IB, 4 as IIA, 1 as IIB, 4 as IIIA, 3 as IIIB, 1 as IV, and 2 as limited small cell carcinoma. Complications occurred in 27% of patients. Operative mortality was 1.7%. CONCLUSION: Computed tomographic screening finds a large number of indeterminate pulmonary nodules in smokers 50 years old or older, most of which are observed and not operated on. Although 47 cancers were detected thus far in this highly selected group of patients, this represents only 1.5% of the pulmonary nodules identified.

Aged↗
PubMed2004

Is there a role for the left ventricle apical-aortic conduit for acquired aortic stenosis?

BACKGROUND AND AIM OF THE STUDY: Aortic valve replacement (AVR) in patients with a heavily calcified ascending aorta and aortic root, or with conditions that preclude a median sternotomy, poses a formidable challenge. A left ventricle apical-aortic conduit (AAC) is an alternative in these situations. Herein, the authors' experience with AAC in adult patients with acquired aortic stenosis is reported. METHODS: Between 1995 and 2003, 13 patients (mean age 71 years) underwent AAC for severe symptomatic aortic stenosis (mean valve area 0.65 +/- 0.02 cm2). Indications for AAC were heavily calcified ascending aorta and aortic root (n = 5), patent retrosternal mammary grafts (n = 4), calcified ascending aorta and aortic root plus patent retrosternal mammary graft (n = 1), retrosternal colonic interposition (n = 1) and multiple previous sternotomies (n = 2). Seven patients had previous coronary artery bypass grafting (CABG). The mean preoperative left ventricular ejection fraction was 50 +/- 4%. RESULTS: AAC were performed under cardiopulmonary bypass through a left thoracotomy (n = 10), median sternotomy (n = 2) or bilateral thoracotomy (n = 1). Hearts were kept beating (n = 5) or fibrillated (n = 7). Circulatory arrest was used in one patient. Composite Dacron conduits with biological (n = 6), mechanical (n = 4) or homograft (n = 2) valves were used. Distal anastomoses were performed in the descending thoracic aorta (n = 12) or in the left iliac artery (n = 1). Two patients underwent simultaneous CABG. Three patients died in-hospital from ventricular failure (n = 1), intravascular thrombosis (n = 1) and multi-organ failure (n = 1). The mean hospital stay was 26 days. Complications included respiratory failure requiring tracheostomy (n = 2), stroke (n = 1) and re-exploration for bleeding (n = 2). At a mean follow up of 2.1 years, there have been four late deaths; causes of death were congestive heart failure (n = 2), ischemic cardiomyopathy (n = 1) and cancer (n = 1). CONCLUSION: AAC provides an acceptable alternative to AVR in selected patients who are at exceedingly high risk for the standard procedure.

Adult↗
PubMed2002

Effect of coenzyme Q10 supplementation on mitochondrial function after myocardial ischemia reperfusion.

BACKGROUND: Coenzyme Q10 (CoQ10) protects myocardium from ischemia-reperfusion (IR) injury as evidenced by improved recovery of mechanical function, ATP, and phosphocreatine during reperfusion. This protection may result from CoQ10's bioenergetic effects on the mitochondria, from its antioxidant properties, or both. The purpose of this study was to elucidate the effects of CoQ10 supplementation on mitochondrial function during myocardial ischemia-reperfusion using an isolated mitochondrial preparation. METHODS: Isolated hearts (n = 6/group) from rats pretreated with liposomal CoQ10 (10 mg/kg iv, CoQ10), vehicle (liposomal only, Vehicle), or saline (Saline) 30 min before the experiments were subjected to 15 min of equilibration (EQ), 25 min of ischemia (I), and 40 min of reperfusion (RP). Left ventricular-developed pressure (DP) was measured. Mitochondria were isolated at end-equilibration (end-EQ), at end-ischemia (end-I), and at end-reperfusion (end-RP). Mitochondrial respiratory function (State 2, 3, and 4, respiratory control index (RCI, ratio of State 3 to 4), and ADP:O ratio) was measured by polarography using NADH (alpha-ketoglutarate, alpha-KG)- or FADH (succinate, SA)-dependent substrates. RESULTS: CoQ10 improved recovery of DP at end-RP (67 +/- 11% in CoQ10 vs 47 +/- 5% in Vehicle and 50 +/- 11% in Saline, P < 0.05 vs Vehicle and Saline). CoQ10 did not change preischemic mitochondrial function. IR decreased State 3 and RCI in all groups using either substrate. CoQ10 had no effect in the mitochondrial oxidation of alpha-KG at end-I. CoQ10 improved State 3 at end-I when SA was used (167 +/- 21 in CoQ10 vs 120 +/- 10 in Saline and 111 +/- 10 ng-atoms O/min/mg protein in Vehicle, P < 0.05). Using alpha-KG as a substrate, CoQ10 improved RCI at end-RP (4.2 +/- 0.2 in CoQ10 vs 3.2 +/- 0.2 in Saline and 3.0 +/- 0.3 in Vehicle, P < 0.05). Using SA, CoQ10 improved State 3 (181 +/- 10 in CoQ10 vs 142 +/- 9 in Saline and 140 +/- 12 ng-atoms O/min/mg protein in Vehicle, P < 0.05) and RCI (2.21 +/- 0.06 in CoQ10 vs 1.85 +/- 0.11 in Saline and 1.72 +/- 0.08 in Vehicle, P < 0.05) at end-RP. CONCLUSIONS: The cardioprotective effects of CoQ10 can be attributed to the preservation of mitochondrial function during reperfusion as evidenced by improved FADH-dependent oxidation.

Animals↗
PubMed2002

Ischemic preconditioning improves mitochondrial tolerance to experimental calcium overload.

BACKGROUND: Ca(2+) overload leads to mitochondrial uncoupling, decreased ATP synthesis, and myocardial dysfunction. Pharmacologically opening of mitochondrial K(ATP) channels decreases mitochondrial Ca(2+) uptake, improving mitochondrial function during Ca(2+) overload. Ischemic preconditioning (IPC), by activating mitochondrial K(ATP) channels, may attenuate mitochondrial Ca(2+) overload and improve mitochondrial function during reperfusion. The purpose of these experiments was to study the effect of IPC (1) on mitochondrial function and (2) on mitochondrial tolerance to experimental Ca(2+) overload. METHODS: Rat hearts (n = 6/group) were subjected to (a) 30 min of equilibration, 25 min of ischemia, and 30 min of reperfusion (Control) or (b) two 5-min episodes of ischemic preconditioning, 25 min of ischemia, and 30 min of reperfusion (IPC). Developed pressure (DP) was measured. Heart mitochondria were isolated at end-Equilibration (end-EQ) and at end-Reperfusion (end-RP). Mitochondrial respiratory function (state 2, oxygen consumption with substrate only; state 3, oxygen consumption stimulated by ADP; state 4, oxygen consumption after cessation of ADP phosphorylation; respiratory control index (RCI, state 3/state 4); rate of oxidative phosphorylation (ADP/Deltat), and ADP:O ratio) was measured with polarography using alpha-ketoglutarate as a substrate in the presence of different Ca(2+) concentrations (0 to 5 x 10(-7) M) to simulate Ca(2+) overload. RESULTS: IPC improved DP at end-RP. IPC did not improve preischemic mitochondrial respiratory function or preischemic mitochondrial response to Ca(2+) loading. IPC improved state 3, ADP/Deltat, and RCI during RP. Low Ca(2+) levels (0.5 and 1 x 10(-7) M) stimulated mitochondrial function in both groups predominantly in IPC. The Control group showed evidence of mitochondrial uncoupling at lower Ca(2+) concentrations (1 x 10(-7) M). IPC preserved state 3 at high Ca(2+) concentrations. CONCLUSIONS: The cardioprotective effect of IPC results, in part, from preserving mitochondrial function during reperfusion and increasing mitochondrial tolerance to Ca(2+) loading at end-RP. Activation of mitochondrial K(ATP) channels by IPC and their improvement in Ca(2+) homeostasis during RP may be the mechanism underlying this protection.

Adenosine Diphosphate↗
PubMed2002

Giant papillary fibroelastoma of the right atrium: an unusual presentation.

Papillary fibroelastomas are small tumors of the valvular endocardium with a propensity to embolize. Fibroelastomas originating in the nonvalvular endocardium are rare. We report a giant papillary fibroelastoma of the right atrial septum presenting with hemodynamic compromise that resolved after surgical excision. The current literature and the diagnostic and therapeutic strategies are reviewed.

Aged↗
PubMed2002

Mitochondrial function during ischemic preconditioning.

Background. Ischemic preconditioning (IPC) protects the myocardium from ischemia reperfusion injury. The effect of IPC on the mitochondria is not well known. However, one of the mechanisms postulated in IPC (the opening of the mitochondrial K(ATP) channels) is likely to result in changes in mitochondrial function. Therefore, the purpose of this study was to determine the effect of IPC on mitochondrial function during ischemia reperfusion. Methods. Isolated rat hearts (n = 6/group) were subjected to (1) 30 minutes of equilibration, 25 minutes of ischemia, and 30 minutes of reperfusion (RP) (control group) or (2) 10 minutes of equilibration, two-5 minute episodes of IPC (each followed by 5 minutes of re-equilibration), 25 minutes of ischemia, and 30 minutes of RP (IPC group). Left ventricular rate pressure product (RPP) was measured. At end-equilibration (end-EQ) and at end-reperfusion (end-RP) mitochondria were isolated. Mitochondrial respiratory function (state 2, 3, and 4), respiratory control index (RCI), rate of oxidative phosphorylation (ADP/Delta t), and ADP:O ratio were measured by polarography with the use of NADH- or FADH-dependent substrates. Results. IPC improved recovery of RPP at end-RP (72% +/- 5% in IPC vs 30% +/- 4% in control, P <.05). Ischemia reperfusion (IR) decreased state 3, ADP/Delta t, and RCI in both groups compared with end-EQ. IPC improved state 3 (47 +/- 3 in IPC vs 37 +/- 2 ng-atoms O/min/mg protein in control), ADP/Delta t (17 +/- 1 in IPC vs 13 +/- 1 nmol/s/mg protein in control), and RCI (3.7 +/- 0.1 in IPC vs 2.1 +/- 0.2 in control) at end-RP compared with control with the use of NADH-dependent substrate (P <.05 vs control). IPC also improved state 3 (85 +/- 6 in IPC vs 71 +/- 4 ng-atoms O/min/mg protein in control), ADP/Delta t (18 +/- 2 in IPC vs 12 +/- 1 nmol/s/mg protein in control), RCI (2 +/- 0.1 in IPC vs 1.5 +/- 0.1 in control), and ADP:O ratios (1.4 +/- 0.04 in IPC vs 1.7 +/- 0.09 in control) at end-RP compared with control with the use of FADH-dependent substrate (P <.05 vs control). Conclusions. The cardioprotective effects of IPC can be attributed at least in part to the preservation of mitochondrial function during reperfusion.

Adenosine Triphosphate↗