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A case of astemizole-induced QT prolongation, T-wave alternans, and torsades de pointes is presented. Failed treatment with intravenous magnesium and lidocaine was followed by overdrive pacing, which successfully prevented further recurrences. The possible pathophysiology of acquired QT syndrome and T-wave alternans after antihistamine use is discussed.

Amiodrone is a benytfuran derivative with class III anti arrhythmic effects. It has also been reported to convert atrial fibrillation and flutter to sinus rhythm and is highly effective for the prevention of atrial fibrillation (especially of the paroxysmal form) with an overall efficacy in the range of 70–50%. This high degree of efficacy was obtained in a majority of patients who had already failed various conventional anti arrhythmic agents. The mechanism of arrhythmia termination by intravenous amiodarone is not clear. The slowing in ventricular response, which most probably improves cardiac hemodynamics, has an indirect salutary effect. Despite the fact that none of the published reports on intravenous amiodarone used a placebo control group, these studies suggest that intravenous amiodarone has an important role in the acute treatment of atrial fibrilation with fast ventricular response.

A patient with clinically silent mitral valve prolapse experienced an episode of out-of-hospital cardiac arrest due to ventricular fibrillation. This arrhythmia was easily replicated in the electrophysiology laboratory and despite treatment with amiodarone alone and amiodarone in combination with propranolol. Amiodarone in combination with quinidine prevented the induction of ventricular fibrillation and proved effective during a 3-year follow-up period. Even though a clear-cut relationship between the arrhythmias and mitral valve prolapse cannot be established, this case suggests that sudden death can occur in patients with mitral valve prolapse but without the known risk factors for the development of sudden death.

Forty patients with recurrent syncopal episodes of uncertain etiology were evaluated with a 60-degree head-up tilt table test for 60 minutes. There were 21 men and 19 women, with a mean age of 36 ± 19 years, a mean of 7.6 syncopal episodes per patient, and a mean duration of symptoms of 4.2 ± 6 years. Twelve patients had evidence of organic heart disease. Ten control subjects with no history of syncope were studied similarly. Syncope did not occur in any of these controls. Syncope occurred in 15 patients (37.5%) after a mean standing time of 42 ± 12 minutes. Syncope was due to a typical vasovagal reaction in 11 patients and to hyperventilation in three patients. One last patient fainted without changes in heart rate or blood pressure. In each case, symptoms during the test resembled those prevlously experienced.

We report on twelve patients with alternating Wenckebach periods (AWP) occurring during an acute inferior myocardial infarction (AIMI). There were nine males and three females, with a mean age of 61 years (range, 43 to 75). AWP appeared during the first 48 hours of the AIMI in 10 patients and on the fourth day of hospitalization in two patients. AWP occurred spontaneously in nine patients and following the administration of atropine in the remaining three patients. Mean systolic blood pressure significantly decreased during AWP as compared to the period preceding or following the bradyarrhythmia (93 +/- 42 mmHg vs 123 +/- 37 mmHg, p less than 0.02). Killip functional class was significantly higher during AWP as compared to the period preceding or following the bradyarrhythmia (2.1 +/- 1.2 vs 1.5 +/- 0.8, p less than 0.02). Pacemaker therapy was initiated prophylactically in two patients, because of syncope in six, because of hemodynamic deterioration in two, and for syncope and hemodynamic deterioration in two. Three patients died in cardiogenic shock despite pacemaker therapy. No evidence of right ventricular infarction was seen in the patients. Atropine administration during AWP significantly increased the sinus rate and significantly decreased the ventricular rates and the systolic blood pressure. In addition, three patients developed long bouts of paroxysmal AV block. Isoproterenol administration improved AV conduction in one patient, caused no change in two patients and induced non-sustained ventricular tachycardia in three patients. In conclusion, AWP occurring during AIMI is a symptomatic bradyarrhythmia associated with hemodynamic deterioration.(ABSTRACT TRUNCATED AT 250 WORDS)

A patient had repetitive ventricular fibrillation preceded by alternating ST segment depression and elevation. The ECG changes were confined to the precordial leads only, reflecting subendocardial and transmural ischemia, respectively. It is speculated that the patient exhibited consecutive episodes of subtotal and total coronary occlusion, both episodes being critical enough to induce lethal arrhythmias.

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.

The effect of intravenous (IV) amiodarone (300 mg) on heart rate was investigated in 22 patients with acute myocardial infarction (18) or ischemia (4) and sinus tachycardia. There were 11 men and 11 women (age range, 48 to 83 years; mean, 63.5). Amiodarone IV slowed the mean heart rate from 109 +/- 14 beats/min to 94 +/- 15 beats/min (p less than 0.0005). There was a linear correlation between the initial heart rate (preamiodarone) and the final heart rate (postamiodarone), (r = 0.6930, p less than 0.0005). Most of the patients with initial heart rates higher than the mean maintained relatively high heart rates (above the mean), while most patients with lower initial heart rates showed low heart rates (below the mean) after amiodarone administration. Patients in Killip class 1 showed a significant reduction in heart rate after receiving amiodarone, from a mean of 105 +/- 10 to 88 +/- 11 beats/min (p less than 0.01). Patients in Killip class 2 also had reduced heart rates (118 +/- 14 to 81 +/- 39 beats/min), but these changes were not statistically significant. Of the three patients in Killip class 3 to 4, the heart rate slowed by 10 beats/min in one, while in the remaining two no changes were observed. There were no significant side effects from the administration of amiodarone.

Thirty-two consecutive patients who initially had horizontal or downward-sloping ST segment depression confined to the precordial leads were studied. Patients were divided into two groups: group A included 21 patients with horizontal or downward-sloping ST depression with peaked positive T waves, and group B comprised 11 patients with peaked negative T waves and downward or horizontal ST depression. The incidence of acute myocardial infarction (AMI) was similar (group A 38.1% vs group B 36.4%; p greater than 0.05). In-hospital mortality was much more significant in group B (p = 0.03). Coronary arteriography was performed in 31 patients. Of the 10 patients in group B who were catheterized, seven (70%) had left main occlusion. Of the 21 patients in group A, none had a significant left main lesion (p = 0.001), although eight (38.1%) had single-vessel disease (p = 0.05). Thus the ECG pattern of horizontal or downward-sloping ST depression passing into a peaked negative T wave identifies a subgroup of high-risk patients in whom the prognosis is poor once AMI occurs. Early catheterization is recommended when this ischemic pattern is apparent on the ECG.

Of 760 consecutive cases with anterior acute myocardial infarction (AMI), 55 developed acute bundle-branch block (BBB), fascicular block, or high-degree atrioventricular block during the hyperacute ECG stage of AMI. According to the direction of the ST segment during the acute ischemic episode, patients were divided into two groups. Group A consisted of 32 patients who developed BBB during ST-segment elevation, positive T wave, and absent or minimal Q wave. Group B consisted of 23 patients who developed BBB during ST-segment depression and evolved into anterior AMI. Group A was characterized by a higher incidence of right BBB and left anterior hemiblock [91% vs. 26% and 56% vs. 13%, respectively (p

E STABLISHING the correct diagnosis for the causative mechanism of syncope is still a medical challenge. Since syncope may be caused by a variety of mechanisms, and since usually the patient arrives for medical attention after the episode has subsided, establishing the proper diagnosis is a difficult task that requires the performance of a variety of tests to rule out possible causes. In addition, since syncope may imply such a variable prognosis, the need to make a correct diagnosis is mandatory. Carotid sinus hypersensitivity (CSH) is a known cause of syncope. Even though it was described long ago, it was not until recent years that its presence and significance became more widely recognized. Nonetheless, we believe that CSH is still a relatively overlooked cause of syncope.’ This is partly related to the difficulty of establishing a clear-cut cause and effect relationship between CSH demonstrated at bedside or in the laboratory, and the patient’s previous syncopal attacks.

This study was designed to evaluate the effects of metaraminol (Aramine) in six patients with evolving acute inferior wall myocardial infarction accompanied by hypotension and warm limbs. There were 16 episodes of acute inferior wall ischemia, and the response to therapy was judged by evaluating blood pressure and ST segment and T wave abnormalities. Three patients received intravenous isosorbide dinitrate and two received streptokinase as the initial therapy. The mean ST segment elevation was significantly reduced (from 4.94 +/- 1 to 0.5 +/- 0.7 [p less than 0.0001]) after metaraminol infusion was initiated. The average T wave height also decreased (from 6.8 +/- 2 to -1.3 +/- 2.5 mm [p less than 0.0005]). The average heart rate decreased from 82 +/- 11 to 69 +/- 9 beats/min (p less than 0.05) and the mean arterial blood pressure increased from 81 +/- 12 mm Hg before metaraminol treatment to 126 +/- 8 mm Hg after treatment. All these changes occurred within a few minutes after metaraminol therapy was instituted. In 12 episodes, accelerated idioventricular rhythm appeared concomitantly with the resolution of ST segment elevation. Coronary angiography performed between 4 and 10 days after admission demonstrated significant obstruction in all infarct-related arteries, but none was totally occluded. Left ventricular function was normal in three patients and slightly hypokinetic in the inferior wall in two. These results indicate that in a selected group of patients with acute inferior myocardial infarction, metaraminol administration (in certain hemodynamic circumstances) can alleviate acute ischemia within a few minutes and thereby reduce ischemic injury.

A severe case of flecainide-induced incessant ventricular arrhythmias is presented. These arrhythmias were resistant to various intravenous antiarrhythmic drugs and to cardiac pacing. Intravenous amiodarone administered over a short period and in a high dose strikingly abolished all ventricular arrhythmias.