Evaluation of hibernating myocardium in patients with ischemic heart disease.

Patients with ischemic heart disease and significant left ventricular dysfunction are often difficult to manage medically. Revascularization procedures may improve left ventricular function and prognosis in this population if hypocontractile yet viable myocardium (hibernating myocardium) is demonstrated. Nuclear cardiology studies (single photon and positron methods), two-dimensional echocardiography, and magnetic resonance imaging studies have been utilized to identify hibernating myocardium. If thallium-201 studies are performed, the use of reinjection of thallium and repeat imaging improves the sensitivity of these studies for the detection of viable myocardium. Dobutamine echocardiographic studies may have a higher specificity and positive predictive value for the subsequent improvement of regional systolic left ventricular function after revascularization than the nuclear techniques. However, thallium studies have an excellent negative predictive value. Positron emission tomography (PET) allows the simultaneous assessment of perfusion and metabolic activity; however, these studies are expensive and not widely available. Functional evaluation with PET is in its infancy. Functional cardiac magnetic resonance imaging (MRI), although not widely available yet, provides the most accurate evaluation of regional ventricular function. MRI spectroscopy may be utilized to assess myocardial viability. As acquisition times improve and "real-time" imaging becomes a reality, MRI and MRI spectroscopy will likely become very accurate tools for assessing functional reserve and metabolic activity. The selection of the most appropriate method for assessment of myocardial viability will include consideration of a patient's characteristics, the presence of coronary arterial tree amenable to revascularization techniques, the techniques available to the clinician to assess viability, and local revascularization experience in this population. The result of an individual patient's evaluation is relevant to the consideration of coronary revascularization, or if this is not possible, cardiac transplantation.

Association of noninvasive markers of coronary artery reperfusion to assess microvascular obstruction in patients with acute myocardial infarction treated with primary angioplasty.

Early restoration of coronary artery patency through primary angioplasty limits infarct size and improves survival. Increasing evidence, however, suggests that microvascular obstruction is often present despite coronary artery recanalization. This may limit the benefits of reperfusion therapy. We studied the use of noninvasive markers of coronary artery reperfusion as indicators of microvascular obstruction and determinants of prognosis in 98 patients with acute myocardial infarction (AMI) who were successfully treated with primary angioplasty (Thrombolysis In Myocardial Infarction grade 3 flow and residual stenosis <30%). Plasma creatine kinase (CK) levels and 12-lead electrocardiograms were performed on admission, at 90 minutes, and at 6, 12, and 24 hours after treatment. We defined: (1) reperfusion as resolution of ST-segment elevation >50% at 90 minutes, with peak CK levels within 12 hours, and T-wave inversion within 24 hours; and (2) failed reperfusion, as the absence of these parameters. Of the 98 patients studied, 87 (88.8%) had reperfusion and 11 (11.2%) had failed reperfusion. Infarct location was anterior (versus inferior) in 9 patients in the failed reperfusion group (81.8%) compared with 41 patients in the reperfusion group (47.1%) (p <0.01). Congestive heart failure >24 hours after presentation or in-hospital death occurred in 11 patients (12.6%) in the reperfusion group versus 5 (45.5%) in the failed reperfusion group (p <0.01). One-year survival was 96.1% for the reperfusion group and 60.6% for the failed reperfusion group (p <0.0001). We conclude that the association of noninvasive markers of reperfusion better identifies patients with microvascular obstruction among those who had a "successful" primary angioplasty. Evidence of impaired microvascular reperfusion is associated with a poor in-hospital and 1-year outcome.

Intrapulmonary shunting in primary pulmonary hypertension: an observation in two patients treated with epoprostenol sodium.

Continuous intravenous infusion of epoprostenol sodium in selected patients with primary pulmonary hypertension improves symptoms and survival. This report describes two patients with primary pulmonary hypertension treated with epoprostenol in whom intrapulmonary shunting and severe hypoxemia occurred. Intrapulmonary shunting was confirmed by contrast echocardiography showing delayed appearance of bubbles in the left cardiac chambers after peripheral venous injection of agitated saline solution.

[Selection and evaluation of candidate patients for heart transplant]. / Selección y evaluación de pacientes candidatos a trasplante cardíaco.

Cardiac transplantation is now a well-accepted therapy for patients with advanced heart failure. In appropriately selected recipients, it has shown to significantly improve the survival and quality of life. The shortage of appropriate cardiac donor hearts, the costs of cardiac transplantation and its associated long-term medical follow-up, and the potential morbidity and mortality associated with the procedure and with life after transplantation mandates the judicious application of cardiac transplantation to appropriate recipients. A review of current indications, contraindications and evaluation of patients for cardiac transplantation is presented.

Gene polymorphisms for plasminogen activator inhibitor-1/tissue plasminogen activator and development of allograft coronary artery disease.

BACKGROUND: Impaired fibrinolytic activity has been linked to the presence and severity of allograft vasculopathy (Tx CAD). This impairment may be associated with the presence of certain fibrinolytic protein gene polymorphisms. METHODS AND RESULTS: To investigate the relation between donor-specific fibrinolytic protein genotypes and Tx CAD, we identified donor plasminogen activator inhibitor-1 (PAI-1) HindIII and tissue plasminogen activator (TPA) EcoRI restriction fragment length polymorphisms-based genotypes by Southern blot analysis in 48 recipients of cardiac allografts and correlated these genotypes with the development of CAD. No association was found between donor TPA genotypes and the presence of Tx CAD. Among the 48 patients, 17% were homozygous for the 1/1 PAI-1 genotype, 51% for the 2/2 PAI-1 genotype, and 32% for the 1/2 PAI-1 genotype. The actuarial freedom from any CAD for the recipients with each respective donor PAI-1 genotype at 12 and 24 months was 100% and 100% for the 1/1 PAI-1 genotype, 92% and 92% for the 1/2 PAI-1 genotype, and 75% and 45% for the 2/2 PAI-1 genotype (P=0.03). Recipients with a diseased 2/2 PAI-1 genotyped allograft had longer ischemic times (P=0.02) than those recipients with a Tx CAD-free allograft. CONCLUSIONS: These data suggest that recipients with a 2/2 PAI-1 genotype are at a significant risk of developing Tx CAD. This genotype may serve as a useful screening tool for predicting the future development of Tx CAD.