[Non-compacted cardiomyopathy: an uncommon cause of ventricular tachycardia]. / Miocardiopatía no compactada: una causa poco frecuente de taquicardia ventricular.

We present the case of a patient who was previously diagnosed of hypertrophic cardiomyopathy. The patient was admitted to our coronary unit due to a sustained ventricular tachycardia picture. A coronariography was performed as part of the ventricular tachycardia study protocol. It showed angiographically normal epicardic arteries. In the ventriculography, there was a pattern of dilated cardiomyopathy with prominent left ventricular trabeculation, which suggested the diagnosis of non-compacted cardiomyopathy (NCC). The findings of the transthoracic echocardiography, that showed a dilated and hypertrophic left ventricle, with very depressed systolic function, and ventricular myocardium with a thick internal non-compacted endocardium, with a meshwork of multiple trabeculations and intracardic recesses in communication with the ventricular cavity, confirmed this diagnosis. There continues to be little knowledge on NCC and thus it is probably underdiagnosed. It must be considered in the differential diagnosis of patients diagnosed of hypertrophic or dilated cardiomyopathy.

Miocardiopatía no compactada: una causa poco frecuente de taquicardia ventricular / Non-compacted cardiomyopathy: an uncommon cause of ventricular tachycardia

Presentamos el caso de un paciente, diagnosticado previamente de miocardiopatía hipertrófica, que ingresó en nuestra Unidad Coronaria por un cuadro de taquicardia ventricular sostenida. Como parte del protocolo de estudio de la taquicardia ventricular se le realizó una coronariografía que mostró arterias epicárdicas angiográficamente normales. En la ventriculografía se apreció un patrón de micardiopatía dilatada con llamativa trabeculación del ventrículo izquierdo, sugiriendo el diagnóstico de miocardiopatía no compactada (MNC). Los hallazgos de la ecocardiografía transtorácica, en la que se apreció un ventrículo izquierdo dilatado e hipertrófico con una función sistólica muy deprimida, y un miocardio ventricular con una gruesa capa interna endocárdica no compactada, con una malla de múltiples trabeculaciones y recesos intramiocárdicos en comunicación con la cavidad ventricular, confirmaron este diagnóstico. La MNC sigue siendo una patología poco conocida, y probablemente por ello infradiagnosticada. Hay que considerarla en el diagnóstico diferencial de pacientes afectos de miocardiopatía hipertrófica o dilatada

We present the case of a patient who was previously diagnosed of hypertrophic cardiomyopathy. The patient was admitted to our coronary unit due to a sustained ventricular tachycardia picture. A coronariography was performed as part of the ventricular tachycardia study protocol. It showed angiographically normal epicardic arteries. In the ventriculography, there was a pattern of dilated cardiomyopathy with prominent left ventricular trabeculation, which suggested the diagnosis of non-compacted cardiomyopathy (NCC). The findings of the transthoracic echocardiography, that showed a dilated and hypertrophic left ventricle, with very depressed systolic function, and ventricular myocardium with a thick internal non-compacted endocardium, with a meshwork of multiple trabeculations and intracardic recesses in communication with the ventricular cavity, confirmed this diagnosis. There continues to be little knowledge on NCC and thus it is probably underdiagnosed. It must be considered in the differential diagnosis of patients diagnosed of hypertrophic or dilated cardiomyopathy

[The thrombolytic treatment of acute myocardial infarct in an emergency department]. / Tratamiento trombolítico del infarto agudo de miocardio en el área de urgencias.

INTRODUCTION AND OBJECTIVES: Although the importance of the early use of thrombolytic therapy in acute myocardial infarction has been demonstrated, it is usual to detect an unacceptable delay in its administration. We measured the in-hospital delay and, when it was determined we designed a protocol to reduce it. METHOD: From January-92 to December-94 we performed a prospective analysis of the measured delay for patients with a diagnosis on admission of acute myocardial infarction or unstable angina within 24 hours of the onset of symptoms. To ensure a homogeneous population, we established a triage system: priority I, delay of the therapy not admissible and so immediate administration of thrombolytic agent (performed in the emergency department); priority II, need for a careful evaluation of the risk/benefit ratio for thrombolytic therapy and administration, when indicated, after admission to the coronary care unit, and priority III, thrombolytic therapy whether indicated or contraindicated. All data were evaluated periodically in order to detect possible failures and to correct them. RESULTS: A total of 1,462 patients with a diagnosis of acute myocardial infarction (n = 1,006) or unstable angina (n = 456) were included. The administration of lytic therapy in the emergency department reduced the In-Hospital delay for thrombolysis by 54% from a median of 65 minutes (45 and 110) to 30 minutes (15 and 60) (p < 0.001) in priority I patients (40% of the patients diagnosed with AMI). For all cases with thrombolytic therapy this time was reduced from 87.5 minutes (50 and 155) to 50 minutes (25 and 110) minutes (p < 0.001). CONCLUSIONS: Awareness of our in-hospital delay, establishing a triage system in the emergency department and administering thrombolytic drugs in the this area has made it possible to provide this therapy to selected patients as early as possible.

[A diffuse pulmonary hemorrhage following thrombolytic therapy in an acute myocardial infarct]. / Hemorragia pulmonar difusa tras terapia trombolítica en infarto agudo de miocardio.

A sixty-years-old man was admitted to the hospital because of acute myocardial infarction of anterior location. He had four episodes of ventricular fibrillation each requiring defibrillation and short-term cardiopulmonary resuscitation (less than 10 minutes). He was then managed with thrombolytic therapy, therapeutic doses of heparin and aspirin. He had persistent haemoptysis, chest X-ray revealing a diffuse bilateral alveolar infiltration. There was a continuous decrease in hemoglobin and hematocrit levels, with an evident clinical-radiographic dissociation. Right cardiac catheterisation showed a normal left ventricular function. The single breath carbon monoxide diffusing capacity (DLCOsb) was high, indicative of a diffuse intrapulmonary haemorrhage causing the alveolar infiltration.

[Thrombolysis of thrombosed heart valve prostheses: presentation of 2 cases and review of the literature]. / Trombólisis de prótesis valvulares cardíacas trombosadas: presentación de 2 casos y revisión de la literatura.

Two women aged 38 and 51 years with thrombosed prosthetic heart valves (TPHV) in both tricuspid and mitral positions have been successfully treated with recombinant tissue plasminogen activator (rt-PA), 70 mg over 5 hours, and streptokinase (SK) 2,000,000 U over 10 hours without important complications. Cardiac surgery is the most commonly used therapy for combating this serious complication with a high mortality rate in general. There is controversy over the use of thrombolytics in TPHV. We reviewed the literature concerning treatment in 90 patients with this complication involving the different valve positions. We found an 80% therapeutical success rate, 8% partially successful, and 7% mortality rate. The main complications were of an embolic nature in 17% of cases, although the majority of these were transitory; haemorrhage occurred in 11% but there was only one case needing a transfusion. We conclude that thrombolytics are an efficient therapy in cases of TPHV in any position and should be started as soon as possible after the diagnosis has been confirmed.