[Clinical practice guidelines of the Spanish Society of Cardiology for pulmonary thromboembolism and hypertension]. / Guías de práctica clínica de la Sociedad Española de Cardiología en tromboembolismo e hipertensión pulmonar.

Primary pulmonary hypertension is a progressive disease. Most affected patients are young and middle-aged women. Etiology is unknown, although a familial and genetic factor is present in up to 6% of cases. Endothelial dysfunction and abnormalities in calcium channels of smooth muscle fibers are the present pathogenetics theories. Diagnostic tests try to exclude secondary causes of pulmonary hypertension and to evaluate its severity. Acute vasodilatory test is vital in the selection of treatment. Oral anticoagulation is indicated in all patients. Lung transplant is performed when medical treatment is unsuccessful. Atrial septostomy is an alternative and palliative treatment for selected cases. Chronic thromboembolic pulmonary hypertension is a special form of secondary pulmonary hypertension, clinically undistinguishable from primary primary hypertension, is of mandatory diagnosis because it can be cured with thromboembolectomy. Pulmonary embolism is common in hospitalised patients. The mortality rate for pulmonary embolism continues to be high: up to 30% in untreated patients. The accurate detection of pulmonary embolism remains difficult, as pulmonary embolism can accompany as well as mimic other cardiopulmonary illnesses. Non-invasive diagnostic tests have poor specificity and sensitivity. The D-dimer level and the spiral CT angiography have also been employed as new alternatives and important tools for precise diagnosis of suspected pulmonary embolism. The standard therapy of pulmonary embolism is intravenous heparin for 5 to 10 days in conjunction with oral anticoagulants posteriorly for 3 to 6 months. The incidence of deep venous thrombosis, pulmonary embolism and death due to pulmonary embolism, can be reduced significantly and shown clear benefits only by adoption of a prophylactic strategy with low-molecular-weight-heparins or dextrans in patients at risk.

Manejo del enfermo con miocardiopatía dilatada y miocarditis / Management of the patient with dilated myocardiopathy and myocarditis

La miocardiopatía dilatada (MCD) es una enfermedad intrínseca del miocardio, caracterizada por la dilatación del ventrículo izquierdo o de ambos ventrículos, así como por la disminución de su contractilidad. Es más frecuente en varones en la edad media de la vida, pero debido a que en las fases iniciales suele cursar de forma asintomática, su incidencia puede estar infraestimada. Se han identificado múltiples etiologías causantes de MCD, y todo apunta a que diversos factores pueden influir conjuntamente en producirla. Con frecuencia no se encuentra el agente causal y entonces se denomina MCD idiopática. Su presentación clínica es muy variada, pero la manifestación más frecuente es la insuficiencia cardíaca (IC), que se agrava conforme evoluciona la enfermedad.El manejo de los pacientes con MCD consiste en retrasar la progresión hacia la IC y disminuir la morbimortalidad.La miocarditis es un proceso inflamatorio no isquémico del miocardio, debido a un amplio y heterogéneo grupo de agentes etiológicos con variada distribución geográfica, lo que afecta a la incidencia y prevalencia de la enfermedad. Existe una fase inicial de agresión al miocardio, que suele seguirse de curación o de una segunda fase de inflamación crónica mediada por mecanismos autoinmunes, asociados o no a la persistencia del agente causal. La clínica varía desde la curación completa hasta la evolución hacia MCD. Su tratamiento es sintomático incluyendo el manejo y prevención de las complicaciones. Actualmente se investiga con la terapia inmunosupresora, basándose en la posible perpetuación del daño miocárdico por mecanismos autoinmunes. (AU)

[Pulmonary hypertension: current aspects]. / Hipertensión pulmonar: aspectos actuales.

Primary pulmonary hypertension, although less frequent than secondary forms, represents the true paradigm of this disease. The recent investigations on pulmonary vascular response mechanisms to different stimuli has increased our knowledge about the mechanism of high pulmonary pressure. Molecular biology of the endothelial cell has provided evidence that endothelial injury plus a genetic individual predisposition may be the pathogenic mainstream of this disease. The histologic findings of pulmonary hypertension are still a matter of controversy, although the clinical, epidemiological and prognostic features are better defined. Therapeutically, there has been important advances, specially with various vasodilators, like calciumantagonists, prostacyclin, adenosine and nitric oxide, as well as new routes of administration. In more advance stages of the disease, atrial septostomy (only paliative) and pulmonary or cardio-pulmonary transplantation, are other therapeutic options to consider, after an adequate selection of patients.

[Cardiomyopathies (VII). Natural history of hypertrophic cardiomyopathy]. / Miocardiopatías (VII). Historia natural de la miocardiopatía hipertrófica.

After a short historic review of conceptual developments in hypertrophic cardiomyopathy, the natural history of the disease is analyzed according to each of its morphologic and functional abnormalities. The lack of association between hypertrophic morphology and sudden death is considered. Diastolic dysfunction and LV obstruction, although a frequent cause of dyspnea and heart failure, is not a risk factor for sudden death. Something similar occurs with the infrequent appearance in this disease of contractile failure. Myocardial ischemia is frequent in hypertrophic cardiomyopathy and general prognostic information about it is still lacking. Nevertheless, in young patients with family history of sudden death, a positive Thallium effort test may be a marker of sudden death (without an arrhythmogenic substrate), and may respond to verapamil. Finally, the new knowledge about genetic mutations in hypertrophic cardiomyopathy are analized. We conclude with some futuristic comments about hypertrophic cardiomyopathy.

Echocardiographic assessment of cardiac function in the rabbit: a preliminary study.

A technique for obtaining M-mode echocardiograms in sedated adult rabbits of both sexes, New Zealand and California breeds, is described. Despite the fact that with rabbits there are certain technical difficulties in obtaining the M-mode echocardiograms, our preliminary results indicate that the following measurements could be the most useful and accurate: 1) left ventricular systolic time intervals; 2) right ventricular systolic time intervals; 3) right ventricular end-diastolic dimension; 4) left atrial internal dimension; 5) left ventricular end-diastolic and end-systolic dimensions; 6) systolic slope of the interventricular septum; 7) mid-diastolic partial closure of the mitral valve (EF slope); and 8) systolic slope of the posterior aortic wall.