תוצאת חיפוש

Circadian Fluctuations of the Signal-Averaged ECG

Ehud Goldhammer, Edward Abinader

Cardiology Dept., Bnei-Zion Medical Center and Bruce Rappaport Faculty of Medicine, The Technion, Haifa

Circadian periodicity for the time of onset of acute myocardial infarction has been shown; the early morning peak of infarction coincides with the onset of other related phenomena, including sudden cardiac death, ventricular arrhythmias, thrombotic stroke, etc. Late potentials detected by the signal-averaged ECG are considered to be independent markers of vulnerability to ventricular arrhythmias. The signal-averaged ECG enables the amplifying and recording of small bioelectric signals of cardiac origin, while eliminating extraneous electrical "noise." To determine whether late potentials are themselves subject to circadian influence, 31 patients (age range 41-79) who had had an old or recent myocardial infarction underwent late potential assessment by the signal-averaged ECG. 4 indices were studied: duration of late LPD potentials (LPD), total QRS duration (TQRS), and root mean square voltage of the last 40 msec, and of the last 50 msec (RMS 40 and RMS 50). These indices were assessed 3 times, during the early morning hours, at noon and during the evening. Morning LPD differed significantly from noon and evening LPD and the morning RMS 40 similarly differed from noon and evening values. TQRS and RMS 50, even though remaining in the normal range, also showed a tendency to abnormal values during morning hours. These findings could possibly be related to the early morning incidence peaks of severe ventricular arrhythmia and sudden cardiac death, since abnormal late potentials constitute the physiopathological basis for certain ventricular arrhythmias.

Prosthetic Heart Valve Thrombosis: A 3-Year Experience

Yaron Shapira, Rafael Hirsch, Ruth Jortner, Moshe Nili, Bernardo Vidne, Alex Sagie

Sheingarten Echocardiography Unit and Cardiology Dept., Rabin Medical Center (Beilinson Campus), Petah Tikva and Sackler Faculty of Medicine, Tel Aviv University

A series of 12 patients with 16 episodes of prosthetic heart-valve thrombosis over 3 years is presented. Most episodes affected mitral or tricuspid bileaflet prostheses. All patients were inadequately anticoagulated at the time of thrombosis. The clinical presentation was acute and severe in 6 patients, and subacute or chronic in the rest. Physical examination was suggestive of stuck valves in most cases. Transthoracic echocardiography revealed increased transvalvular gradients in most. However, clearer evidence of valve thrombosis was obtained from transesophageal echocardiography or fluoroscopy. 9 patients eventually had their valves re-replaced successfully, and the preoperative diagnosis was confirmed in all. 5 patients were operated as soon as the diagnosis was established, and an additional 4 were operated after failure of anticoagulation. In 4 patients the valve leaflets became completely mobile after a course of thrombolysis. Prosthetic valve thrombosis is a severe and potentially fatal complication in patients with mechanical heart valves. Alertness of physicians at all levels- the general practitioner, the internist and the cardiologist- to the possibility of valve thrombosis and to its clinical presentation may lead to prompt and earlier diagnosis and to comprehensive therapy.

Ischemic Hepatitis in Congestive Heart Failure after an Episode of Hypotension

Ora Shovman, Jacob George, Yehuda Shoenfeld

Dept. of Medicine B and Autoimmune Disease Clinic Research Unit, Sheba Medical Center, Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv University

Ischemic hepatitis can occur as an acute episode in advanced congestive heart failure (CHF). The mechanism is massive necrosis of the central lobules resulting from acute hypoxia when low cardiac output further reduces oxygen supply, aggravating underlying congestion due to poor venous outflow. We describe a 70-year-old woman with congestive heart failure for 7 years who was admitted with jaundice, vomiting, abdominal pain and oliguria after an episode of hypotension. The diagnosis of ischemic hepatitis was established by a documented episode of severe hypotension, followed by elevation of serum transaminases, a rise in serum bilirubin and LDH levels, prolonged prothrombin time and acute renal failure. Other causes of acute hepatitis, such as a virus or drugs were excluded, and improved liver and renal function followed hemodynamic stabilization. We conclude that ischemic hepatitis should be considered whenever acute hepatitis follows a recent episode of systemic hypotension, especially in the context of concomitant CHF.