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Study Objectives: To assess the consequences of nitrate withdrawal in angina-free and hemodynamically stable coronary patients.Design: Prospective, open, intervention study.Setting: Cardiology outpatient clinic of a university-affiliated municipal hospital.Patients: Angina-free patients who were hemodynamically stable for at least 3 months before study onset were enrolled. They were all regularly receiving nitrates for symptom control. Those with significant reasons to avoid stopping nitrates, such as heart failure (ejection fraction <35%) or high BP (> 160 mm Hg systolic and/or > 100 mm Hg diastolic), and noncompliant patients were excluded.Interventions: After providing informed consent and undergoing an exercise test (whenever possible), the participants were randomized to abruptly discontinue (study group) or continue (control group) nitrate treatment. Follow-up continued for at least 3 months after study entry.Measurements and Results: Eighty patients were randomized to the study group and 40 patients to the control group (mean age [+/- 1 SD], 65.5 +/- 11 years and 66.1 +/- 10.9 years, respectively; p = not significant). The first month, eight study patients (10%) had a recurrence of anginal symptoms, compared with one control subject (2.5%) [p = not significant]. All eight patients responded promptly and favorably to the resumption of nitrate administration.Conclusions: Nitrate administration can be safely discontinued in angina-free and hemodynamically stable coronary patients who receive this medication on a regular basis. If relapse of anginal symptoms occurs, it will be within 1 month following nitrate withdrawal, and will resolve satisfactorily with reinstatement of treatment. [ABSTRACT FROM AUTHOR]

Background: The natural polyamine Agmatine (Ag) plays a significant role in protection of nerve cell ischemic injury. A previous report indicated that Ag given intraperitoneally to rats enhanced the recovery of the heart from ischemic injury. Based on this initial observation, a larger investigation was undertaken to explore a dose-response effect and possible mechanisms underlying the protective effects.Methods: Using the modified Langendorff model, 36 isolated hearts were divided into five groups: group 1, hearts receiving 100 microM/L Ag pre-ischemia (n=7); group 2, hearts receiving 100 microM/L Ag pre- and post-ischemia, (n=7); group 3, hearts receiving 250 microM/L Ag pre-ischemia (n=7); group 4, hearts receiving 250 microM/L Ag pre- and postischemia (n=7); and group 5, hearts receiving Krebs-Hensleit solution served as control (n=8). The study design included 20 minutes of perfusion, 30 minutes of global ischemia, and 30 minutes of reperfusion.Results: After ischemia, group 2 developed higher left ventricular pressure P(max) (P<0.01), improved first-derivative of the rise (dP/dt max; P<0.02), and fall (dP/dt min; P<0.04) in left ventricular pressure, and the area calculated under the left-ventricle developed pressure curve (pressure-time integral; P<0.015), but coronary flow was not significantly increased (P=0.06) compared to the control group. Group 1 had improved diastolic recovery: dP/dt min (P<0.05) and coronary flow (P<0.03), compared with the control group. Group 3 had improved P(max) (P<0.01), dP/dt min (P<0.01), and coronary flow (P<0.02); group 4 had no improvement in all hemodynamic parameters.Conclusion: Low doses of Ag given pre- and post-ischemia, and high doses given only pre-ischemia have favorable, protective effects on the hemodynamic recovery of isolated rat heart undergoing global ischemia and reperfusion. [ABSTRACT FROM AUTHOR]

Aims To evaluate the impact selected risk factors for cardiac death may have on the success rate in a large cohort of subscribers to ‘SHAHAL’ who were resuscitated from out-of-hospital cardiac arrest.Methods and Results In this medical facility currently serving 50000 subscribers, data were prospectively gathered from between 1987–1998. The information retrieved from the patients' medical records included a medical history of hypertension, diabetes, hypercholesterolaemia (>220·mg.dl−1) smoking, angina, previous myocardial infarction, and congestive heart failure. A total of 998 patients aged 74±12 years (mean±1SD) were included. Death was announced at the scene for 659 (66%) victims, while 339 (34%) patients were taken to hospital. Of these 140 (14% of the total cohort) survived and were discharged from the hospital. A comparison of various selected parameters between survivors and non-survivors of resuscitation revealed that survivors were younger, had a higher rate of pulseless ventricular tachycardia/ventricular fibrillation, more were among the arrests witnessed by the ‘SHAHAL’ team, and that more had a shorter time lag to initiation of cardiopulmonary resuscitation than non-survivors. None of the studied risk factors predicted the outcome of cardiopulmonary resuscitation, with the exception of hypercholesterolaemia, which carried a significantly worse prognosis for cardiopulmonary resuscitation (P=0·009).Conclusions A medical history of hypercholesterolaemia appears to be an important risk factor which adversely affects the outcome of cardiopulmonary resuscitation. [ABSTRACT FROM PUBLISHER]

Aims To determine the circadian rhythm of paroxysmal atrial fibrillation in a very large outpatient population.Methods and Results We reviewed all emergency telephone calls received in Shahal (a medical service covering 44000 subscribers), from 1987 to 1997. Patients were included if new-onset atrial fibrillation was recorded. During this study period, 9989 episodes of paroxysmal atrial fibrillation were recorded. The time of onset was not uniformly distributed throughout the 24h period. Instead, the distribution of arrhythmic episodes showed a double peak, with a significant increase in the number of episodes in the morning and a second rise in the evening (P<0·001). A non-uniform weekly distribution of events was also noted, with substantially fewer episodes on Saturdays (P<0·001). Finally, more arrhythmias occurred during the last months of each year (P<0·001).Conclusions The onset of paroxysmal atrial fibrillation does not occur randomly. The large patient population in the present study suggests that the circadian rhythm of paroxysmal atrial fibrillation is similar to that described for other cardiovascular diseases, with clustering of events in the morning and (to a lesser degree) late in the evening. Weekly and yearly circadian patterns are also prominent. [ABSTRACT FROM PUBLISHER]

Electrophysiological studies were carried out in two patients with an idiopathic left bundle branch block. Consistent distal His bundle pacing resulted in the normalization of the QRS complex in both patients. Extrastimulation during basic distal His pacing at several cycle lengths was carried out successfully. Using this technique, the refractory periods of the left bundle branches were measured and found to be within the normal range. In addition, they decreased with the shortening of the basic cycle length. These results demonstrated the possibility of determining the refractoriness of the left bundle branch by His bundle pacing in patients with left bundle branch block. Hypotheses are postulated about the presumed location of the lesion responsible for the left bundle branch block. [ABSTRACT FROM AUTHOR]

A 28-year-old male with recurrent episodes of ventricular fibrillation, which were initiated by very early ventricular premature depolarizations with a normal QT interval, was subjected to three consecutive electraphysiological studies. During the first study, which was carried out to test the efficacy of amiodarone treatment, no ventricular arrhythmias could he induced. While on amiodarone therapy. the patient experienced another syncopal episode and therefore a second electrophysiological study was done. In that study, ventricular fibrillation was induced by ventricular stimulation. During the third study, which was carried out in order to evaluate the effect of the addition of quinidine to the on going amiodarone therapy no more than three repetitive ventricular responses could be induced. The patient has been asymptomatic: since the third study (fifteen months) with combined therapy of amiodarone and quinidine. The significance of the ability to induce ventricular fibrillation during an electrophysiological study is discussed as well as the value of such studies in determining the long-term efficacy of antiarrhythmic drug therapy. [ABSTRACT FROM AUTHOR]

Objective This study was designed to detect changes in complement levels following acute myocardial infarction and to test whether magnesium sulphate (MgSO4 administration interferes with the complement response that follows acute myocardial infarction. Design Twenty-nine patients with acute myocardial infarction treated with streptokinase were included and randomly assigned to three treatment groups. In groups A and B, a bolus of 1 g MgSO4 was infused intravenously followed by 4 g (group A) and 14 g (group B) MgSO4 for 24 h while normal saline was administered in group C (control). Blood samples for C3, C4 and CH-l00 were obtained at baseline and repeatedly during the 48 h following the initiation of magnesium infusion. Results In groups A and C, a remarkable decrease in the levels of C3, C4 and CH-l00 was observed when measured 1 h after the end of streptokinase infusion and thereafter for the ensuing 48 h compared to baseline values (P<0·05). In group B, the decrease in these complement elements was attenuated, and a significant (P<0·05) delayed decrease of C3 and C4 was observed only at 24 h and later up to 48 h. The mean level of CH-l00 in group B was significantly depressed compared to baseline from 3 h and thereafter up to 48 h. Mean C3 values plotted against observation time differed between the three groups (P=0·021). A similar trend was observed for C4 (P=0·133) but not for CH-l00 (P= 0·46). Conclusion (1) Complement elements are being consumed following acute myocardial infarction treated by streptokinase. (2) High-dose intravenous magnesium attenuates the complement process following acute myocardial infarction. (3) These results might signify that magnesium modulates the inflammatory response that follows infarction. [ABSTRACT FROM PUBLISHER]

A 28-year-old man is described with no demonstrable organic heart disease and recurrent paroxysmal attacks of sustained ventricular tachycardia. Lignocaine and ajmaline failed to terminate the first attack but a bolus infection of verapamil succeeded. This drug was subsequently successful on six more occasions. During electrophysiological study of the eighth attack, slow intravenous administration of verapamil significantly reduced the rate of the tachycardia and prevented its subsequent reinitiation by pacing. Two mechanisms are postulated to explain both the arrhythmia and the beneficial effects of verapamil in this case. [ABSTRACT FROM PUBLISHER]

The clinical significance of sustained nonclinical ventricular tachycardia (VT) induced during electrophysiologic studies was studied in 10 amiodarone-treated patients. Nine patients had previous myocardial infarction while 1 patient had right ventricular dysplasia. All patients had only a single morphologic type of VT recorded during the multiple spontaneous episodes of tachycardia. After serial pharmacological electrophysiologic testing, the patients were placed on antiarrhythmic regimens which included amiodarone in cases. These drugs did not prevent the induction of nonclinical VT in any of the 10 patients and of sustained clinical VT in 7 patients. Nonclinical VT was sustained, requiring cardioversion (7 patients) or rapid ventricular pacing (3 patients) for termination. After a mean follow-up period of 27±10 months (range 12 to 36 months), 4 patients did not exhibit recurrent VT, 3 patients with inducible clinical VT experienced recurrent episode of clinical VT after 16, 27 and 49 months, respectively, 2 patients had nonarrhythmia related deaths after 11 and 12 months, and 1 patient died suddenly after 17 months. These results suggest that laboratory induction of sustained nonclinical VT in amiodarone-treated patients does not imply the likelihood of their future spontaneous occurrence and, therefore, their prevention may be required. [ABSTRACT FROM PUBLISHER]

Echocardiography was used in 30 women and 2 men with systemic lupus erythematosus (SLE) in order to determine the incidence and severity of pericardial effusion and mitral valve involvement. 31 patients showed normal thickness of the mitral valve leaflets, only one patient showed irregular thickening of the leaflets suggesting the presence of vegetations. Mitral valve motions were normal in all patients. These results indicate that myocardial and valvular involvement in SLE is usually not severe enough to result in haemodynamic abnormalities. Pericardial effusion was found in 2 patients who were symptom free, whereas 4 of the patients with a past history suggestive of pericarditis showed no echocardiographic evidence of pericardial effusion. These suggest the transient nature of pericarditis in SLE, and the value of echocardiography as a diagnostic tool in detecting clinically inapparent lupus pericarditis. [ABSTRACT FROM PUBLISHER]

Presents a study that evaluated the effects of the theophylline derivative aminophylline during bradyasystolic arrest refractory to conventional therapy. Assessment of the immediate response of the patients to aminophylline; Analysis of the short-term health outcome of the patients studied; Examination of electrocardiographic recordings from the patients.

Objective: To determine whether clonidine can slow ventricular rate in patients with rapid atrial fibrillation.Design: Randomized, controlled trial, with a 4-hour follow-up period.Setting: Emergency room of a university hospital.Patients: A consecutive sample of 18 hemodynamically stable patients who were evaluated or treated for rapid atrial fibrillation. Exclusion criteria included acute or terminal illness; current use of antiarrhythmic agents, calcium-channel blockers, or beta-blockers; excessive hypertension; pulmonary, valvular, or pericardial disease; and electrolyte imbalance.Interventions: Patients were randomly assigned to receive either "no treatment" (control group) or clonidine, 0.075 mg orally, at baseline and after 2 hours if heart rate did not decrease by at least 20%.Measurements: Blood pressure was measured by the same nurse in the same arm for 4 consecutive hours, and a full 12-lead electrocardiographic evaluation was done.Main Results: Heart rate decreased to below 100 beats/min in eight of nine patients receiving clonidine compared with two of nine patients in the control group. The difference in the mean decreases in heart rate was 38 beats/min (95% CI, 20 to 56 beats/min). Six patients who were treated with clonidine and one patient in the control group reverted to normal sinus rhythm. Systolic blood pressure decreased slightly in both groups, without significant differences. Clinical follow-up was uneventful.Conclusion: Low-dose clonidine was an easy, efficient, and effective treatment for patients with rapid atrial fibrillation who were hemodynamically stable. [ABSTRACT FROM AUTHOR]