Are neutrons involved in the pathogenesis of life-threatening cardiac arrhythmias?

Geomagnetic fields protect the earth from the adverse effects of cosmic rays, whose activity can be indirectly measured by monitoring the level of neutrons in the environment. The number and days of discharges from automatic implantable cardioverter defibrillators (ICD) in patients with cardiac arrhythmias are inversely correlated with the daily level of geomagnetic activity (GMA). The aim of the present was to determine whether neutron levels on days of AICD discharges are higher than average. Days on which discharges occurred were recorded in 31 patients bearing ICDs for managing ischemic cardiomyopathy. Daily neutron levels obtained from the monitoring data of the Russian Academy of Sciences in Moscow were analyzed using Student's t test. The mean (+/-SD) daily neutron level for the 1096-day period was 8299.29 +/- 294.236 imp/min (median 8252), and for days of ACID discharge, 8423.93 +/- 274.187 imp/min (median 8443) (p = 0.0002). The mean neutron activity on days of AICD discharges in response to ventricular disturbances was significantly higher than the mean level over the 1096-day study period. Whether this relation is a direct result of low GMA or due to an independent role of neutrons in the pathogenesis and timing of cardiac arrhythmias is unknown.

Sudden death in three teenagers: conduction system studies.

The pathologic substrate for sudden death in the middle-aged or elderly adult is usually ischemic heart disease. In contrast, few data are available regarding the pathology of sudden death in teenagers. This report describes three teenagers without clinically suspected heart disease dying suddenly. Patient 1 (age 15, male) was known to have right ventricular premature ventricular beats. Postmortem examination revealed marked premature aging, sclerosis of the cardiac skeleton extending to the right side of the summit with fibrosis of the left and right bundle branches. Patient 2 (age 17, male) was a trained athlete who died during football scrimmage. Autopsy revealed moderate mitral valve prolapse and marked premature aging, sclerosis of the left side of the cardiac skeleton, which extended to the right ventricular side, and secondary involvement of the trifascicular conduction system with mononuclear cell infiltration. Patient 3 (age 19, female) died suddenly at home. Autopsy revealed mitral valve prolapse, thrombosis of the sinoatrial (SA) node artery, and premature aging, sclerosis of the left side of the cardiac skeleton, with involvement of the ventricular septum more on the right ventricular side and involvement of the atrioventricular bundle and trifascicular conduction system. In conclusion, unexpected deaths in three teenagers occurred with demonstrable pathologic findings in the heart. Two of the three patients had mitral valve prolapse, one of whom also had thrombosis or embolism of the sinoatrial node artery. All three had sclerosis of not only the left side but also the right side of the ventricular septum with involvement of the conduction system. The anatomic substrate demonstrated in these three patients could relate to lethal bradyarrhythmia or tachyarrhythmia, or both.

Effect of metaraminol during acute inferior wall myocardial infarction accompanied by hypotension: preliminary study.

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.

Transient right axis deviation during acute anterior wall infarction or ischemia: electrocardiographic and angiographic correlation.

Eleven patients, three with acute anterior myocardial infarction and eight with anterior ischemia, who developed transient right axis deviation with a left posterior hemiblock pattern during the acute phase of myocardial infarction or ischemia are described (study group). A correlation between their electrocardiographic pattern and the angiographic findings was made. The arteriographic findings were compared with those of a group of 24 patients with acute anterior myocardial infarction or ischemia without transient right axis deviation (control group). The main electrocardiographic characteristics of the right axis deviation pattern were: an average shift of the mean frontal axis to the right of 42 degrees (10 degrees to 94 degrees); increased voltage of R waves in leads II, III and a VF and appearance of small Q waves or decreased voltage of Q waves if previously present in the same leads; decreased voltage of R waves and appearance of deep S waves in lead aVL; and inverted T waves and isoelectric ST segments in leads II, III and aVF. Coronary angiography revealed that the study group had a higher incidence of significant right coronary artery obstruction and collateral circulation between the left coronary system and the posterior descending artery than did the control group (100 versus 25% and 73 versus 0%, respectively; p less than 0.01). There were no differences between the groups regarding left anterior descending and circumflex artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Importance of the conal branch of the right coronary artery in patients with acute anterior wall myocardial infarction: electrocardiographic and angiographic correlation.

OBJECTIVES: This study assessed prospectively the correlation between the conal branch of the right coronary artery and the pattern of ST segment elevation in leads V1 and V3R during anterior wall acute myocardial infarction (AMI). BACKGROUND: The traditional electrocardiographic (ECG) definition of anteroseptal AMI-ST segment elevation in leads V1 to V3-has recently been challenged. The significance of ST segment elevation in lead V1 during anterior wall AMI is unclear. METHODS: The admission 12-lead ECG with additional lead V3R and the coronary angiograms performed within 10 days of hospital admission were evaluated in 28 consecutive patients (mean age +/- SD 62 +/- 9 years) admitted to the coronary care unit with anterior wall AMI. Patients were classified into two groups according to the magnitude of ST segment elevation in lead V1: group A (elevation > or = 1.5 mm, n = 12) and group B (elevation < 1.5 mm, n = 16). Two types of conal branch were identified: small (not reaching the interventricular septum [IVS]) and large (reaching the IVS). RESULTS: ST segment elevation in lead V3R was found in 11 (92%) and 6 (37%) patients from group A and group B, respectively (p < 0.001); a small conal branch was seen in 10 (83%) and 3 (19%) patients, respectively (p < 0.001). Ten patients (all from group B) had a large conal branch. CONCLUSIONS: ST segment elevation in lead V1 in the admission ECG of patients with anterior wall AMI is strongly related to ST segment elevation in lead V3R and is associated with a small conal branch. Our findings suggest that lead V1 reflects the right paraseptal area supplied by the septal branches of the left anterior descending coronary artery (LAD), alone or together with the conal branch. The absence of ST segment elevation in lead V1 during anterior AMI suggests that the IVS is protected by a large conal branch in addition to the septal branches of the LAD (double circulation).

Thrombolysis is an effective and safe therapy in stuck bileaflet mitral valves in the absence of high-risk thrombi.

OBJECTIVES: We sought to evaluate the effectiveness and safety of thrombolytic therapy in stuck mitral bileaflet heart valves in the absence of high-risk thrombi. BACKGROUND: Current recommendations for the thrombolytic treatment of stuck prosthetic mitral valves are partially based on older valve models and inclusion of patients in whom high-risk thrombi were either ignored or not sought for. The feasibility and safety of thrombolysis in bileaflet models may be affected by the predilection of thrombi to catch the leaflet hinge. METHODS: We studied 12 consecutive patients (men/women = 5/7, age 58.8 +/- 14.9 years) who experienced one or more episodes of stuck bileaflet mitral valve over a 33-month period and received thrombolytic therapy with streptokinase, urokinase or tissue-type plasminogen activator. Transesophageal echocardiography was performed in all patients. Patients with mobile or large (>5 mm) thrombi were excluded. Functional class at initial episode was I-II in 4 patients (33.3%) and III-IV in 8 patients (66.6%). RESULTS: Patients receiving thrombolytic therapy achieved an overall 83.3% freedom from a repeat operation or major complications (95% confidence interval 51.6-97.9%). Minor bleeding occurred in three patients (25%) and allergic reaction in one (8.3%). Transient vague neurologic complaints, without subjective findings, occurred in four patients (33.3%). Three patients had one or more relapses within 5.2 +/- 3.1 months from the previous episode, and readministration of thrombolytics was successful. CONCLUSIONS: In clinically stable patients with stuck bileaflet mitral valves and no high-risk thrombi, thrombolysis is highly successful and safe, both in the primary episode and in recurrence. The best thrombolytic regimen is yet to be established.

Long-term follow-up of patients receiving aprindine. Safety and efficacy.

Aprindine hydrochloride is an antiarrhythmic agent presently undergoing clinical trials in the United States. Because of the narrow therapeutic-toxic ratio observed for aprindine, the long-term follow-up of these patients is important in determining the potential clinical effectiveness of this drug. In this report we examine our experience with 30 patients with drug-resistant arrhythmias who were discharged receiving aprindine and who were followed up for a mean period of 25 months.

Polymorphous ventricular tachycardia: clinical features and treatment.

Thirty-four cases of ventricular tachyarrhythmia characterized by polymorphy of the QRS complexes with changing R-R intervals and a heart rate of 150 to 300 beats/min, termed polymorphous ventricular tachycardia, are described. The factors involved in the appearance of this arrhythmia were the administration of antiarrhythmic drugs (quinidine 22 patients, procainamide 5 patients, ajmaline 1 patient), antianginal drugs (prenylamine [Synadrin] 4 patients) and antidepressant drugs (thioridazine 1 patient). Twenty-one patients were treated for premature ventricular complexes, three for chronic recurrent ventricular tachycardia, six for atrial flutter and fibrillation, three for anginal pain and one patient for mental depression. All patients except one had a drug-induced prolonged corrected Q-T interval before the appearance of polymorphous ventricular tachycardia. Most of the patients with this arrhythmia were considered to have severe myocardial disease. Lidocaine and electric cardioversion were administered to all patients, but were effective only in seven patients whose tachycardia occurred in short, single episodes. The most effective treatment (17 patients) was temporary ventricular pacing at rates ranging from 100 to 140 beats/min. Intravenous isoproterenol proved to be successful in another 10 cases. It is concluded that patients with severe myocardial involvement receiving antiarrhythmic drugs for premature ventricular complexes, especially the multiform variety, are at high risk for the development of polymorphous ventricular tachycardia.

Long-term follow-up of postmyocardial infarction patients with ventricular tachycardia or ventricular fibrillation treated with amiodarone.

Amiodarone in a low dose (200 mg/day) was administered alone or in combination with other type I antiarrhythmic drugs as a first-line agent in 33 patients with ventricular tachycardia (VT) (n = 24) or ventricular fibrillation (VF) (n = 9) secondary to coronary artery disease with healed myocardial infarction. There were 30 men and 3 women (mean age 69 +/- 9 years). Left ventricular ejection fraction ranged from 16 to 45% (mean 29 +/- 8). Therapy was guided by the results of electrophysiologic studies without the use of a control study (without drugs). Predischarge electrophysiologic studies revealed inducible sustained VT in 8 patients (24%), nonsustained VT in 7 and noninducible VT in 18 patients. Mean follow-up time was 27 +/- 7 months. Eleven patients (33%) died, 5 suddenly (15%) and 6 from nonarrhythmic causes. Five patients (15%) had nonfatal recurrences of VT. Life-table analysis showed that arrhythmic recurrences or fatalities (VT or sudden death) were related to the results of the predischarge electrophysiologic studies and not to the baseline arrhythmia (VT or VF). Toxicity from amiodarone was uncommon and no patient discontinued taking the drug.

Amiodarone-induced thyroid gland dysfunction.

Of a population of 400 patients treated with amiodarone, 97 underwent thyroid function evaluation. Of these, 20 patients proved to be thyrotoxic and 16 hypothyroid. In thyrotoxic patients, symptoms developed 2 to 36 months after starting treatment with amiodarone, the most specific laboratory finding being a high total T3 (TT3). No antithyroid treatment proved useful. Thyroid function returned to normal 3 to 7 months after stopping amiodarone therapy. In the hypothyroid group, a high thyroid-stimulating hormone was the most specific laboratory finding. These patients were treated with substitute therapy with or without withdrawal of amiodarone. The iodine content of the thyroid gland in part of this population taking amiodarone was measured by in vivo x-ray fluorescence. Patients in whom thyrotoxicosis developed showed especially high iodine contents. During treatment with amiodarone, patients at high risk of thyrotoxicosis were recognized by increasing TT3 values and higher iodine thyroid levels. A reduction in maintenance dose should be considered in this specific population.

Aprindine-induced polymorphous ventricular tachycardia.

Five cases of aprindine-induced polymorphous ventricular tachycardia (torsade de pointes) are presented. In four cases, polymorphous ventricular tachycardia appeared after the oral administration of 400 mg of aprindine. One patient had mild hypokalemia at the time of polymorphous ventricular tachycardia so that a direct cause and effect relation between the drug and the tachycardia cannot be established. All five patients manifested Q-T prolongation and recurrent syncope due to polymorphous ventricular tachycardia. In all five, polymorphous ventricular tachycardia subsided once administration of aprindine was discontinued.

Effects of isosorbide dinitrates intravenously in high doses over a short period in anterior acute myocardial infarction.

The effects of intravenous isosorbide dinitrate administered in high doses over a short period of time in 17 patients (14 men, 3 women, mean age 67 years) with anterior wall acute myocardial infarction were evaluated. Patients were classified into 2 groups based on the electrocardiographic pattern of acute ischemia. Patients presented with anterior acute myocardial infarction; an electrocardiographic pattern of third-degree ischemia demonstrated a more favorable electrocardiographic and radionuclear angiographic evolution than similar patients who presented with an electrocardiographic pattern of second-degree ischemia.

Prognostic significance of maximal precordial ST-segment depression in right (V1 to V3) versus left (V4 to V6) leads in patients with inferior wall acute myocardial infarction.

This study examines whether patients with inferior wall acute myocardial infarction (AMI) and maximal ST-segment depression in left precordial leads are at higher risk for in-hospital mortality. The charts of patients (n = 213) with inferior wall AMI and an initial electrocardiogram that displayed peaked, tall T waves or ST-segment elevation with upright T waves in inferior leads were reviewed, after excluding patients with inverted T waves in inferior leads (n = 75). ST-segment deviation from baseline was measured for all leads. Patients were classified into 3 types: I = no precordial ST-segment depression; II = sum of ST-segment depression in leads V1 to V3 equal to or more than the sum of ST-segment depression in leads V4 to V6; and III = maximal precordial ST-segment depression in leads V4 to V6. Thirty-six patients (17%) died in the hospital. In-hospital mortality rates for patients with types I and II were 12% and 10%, respectively, compared with 41% for those with type III (p < 0.0001). Mortality rates in surviving patients were similar for all types up to 1 year after infarction. Multivariate logistic regression models for in-hospital mortality by ST-segment depression type adjusted for age, previous AMI, diabetes mellitus, and thrombolytic therapy revealed that type III pattern was a strong predictive factor for in-hospital mortality (odds ratio = 4.9, p = 0.0008, 95% confidence interval 1.93 to 12.26). Thus, patients with inferior wall AMI and maximal precordial ST-segment depression in leads V4 to V6 are at high risk for in-hospital mortality.

Clinical significance and predisposing factors to symptomatic bradycardia and hypotension after percutaneous transluminal coronary angioplasty.

Of 180 consecutive patients who underwent uneventful percutaneous transluminal coronary angioplasty (PTCA), 25 (13.9%) had at least 1 episode of symptomatic bradycardia and hypotension during the early postprocedure period. Symptomatic bradycardia and hypotension occurred 1 to 10 hours (mean 4 +/- 2) after PTCA. A higher incidence of symptomatic bradycardia and hypotension was found in patients receiving regular treatment with beta blockers (26% vs 10% in patients without beta blockers in their regimen, p < 0.01), diltiazem or verapamil (20% vs 9%, p < 0.025), or both a beta blocker and diltiazem or verapamil (64% vs 11%, p < 0.001). A higher incidence was also associated with angioplasty of the left anterior descending coronary artery compared with angioplasty of the other coronary arteries (22% vs 8%, p < 0.01). It is concluded that symptomatic bradycardia and hypotension is a common occurrence after PTCA. The incidence is higher after PTCA to the left anterior descending coronary artery and in patients receiving diltiazem, verapamil, and beta-blocking agents; it is particularly high in patients receiving a combination of a beta-blocking agent and either diltiazem or verapamil.

Importance of left anterior hemiblock development in inferior wall acute myocardial infarction.

Of the 87 consecutive patients admitted with first inferior wall acute myocardial infarction, 17 had acute left anterior hemiblock. The appearance of left anterior hemiblock identified a specific group with more extensive coronary artery disease and suggests disease of the left anterior descending coronary artery.

Comparison of patients with inferior wall acute myocardial infarction with versus without ST-segment elevation in leads V5 and V6.

One hundred forty-one patients with first acute inferior wall myocardial infarction were examined. ST-segment elevation in precordial leads V5 to V6 was found in 34; 94% of them had "mega-artery" compared with 2% in those without ST-segment elevation in precordial leads V5 to V6.

Retrograde dual atrioventricular nodal pathways.

Thirty-one (3.5 percent) of 887 studied patients had retrograde dual atrioventricular (A-V) nodal pathways, as manifested by discontinuous retrograde A-V nodal conduction curves (29 patients) or by two sets of ventriculoatrial (V-A) conduction intervals at the same cycle length (2 patients). All patients had A-V nodal reentrant ventricular echoes of the unusual variety induced with ventricular stimulation (25 patients had single, 2 patients had double and 4 patients had more than three ventricular echoes). The weak link of the reentrant circuit was always the retrograde slow pathway. Eleven of the 31 patients also had anterograde dual A-V nodal pathways (bidirectional dual pathways). Eight patients (26 percent) had spontaneous as well as inducible A-V nodal reentrant paroxysmal supraventricular tachycardia (of the unusual type in three and the usual type in five). In addition, three patients (10 percent) had only inducible supraventricular tachycardia (two of the unusual and one of the usual type). Retrograde dual A-V nodal pathways are uncommon. They are associated with the finding of at least single A-V nodal reentrant ventricular echoes (all patients), anterograde dual pathways (one third of patients) and A-V nodal reentrant paroxysmal supraventricular tachycardia of the usual and unusual variety (one third of patients).

Paroxysmal atrial flutter and fibrillation associated with preexcitation syndrome: treatment with ajmaline.

Ajmaline was administered intravenously to six patients with the Wolff-Parkinson-White syndrome for the acute management of paroxysmal atrial flutter (three patients) or fibrillation (three patients) with a fast ventricular response (over the accessory pathway). Ajmaline increased refractoriness in the accessory pathway in all three patients with atrial flutter and stopped the flutter in one. The drug completely abolished preexcitation in two of the three patients with atrial fibrillation, decreasing the means ventricular rate of 240 and 300 beats/min to 110 and 180 beats/min, respectively. In the third patient with atrial fibrillation, ajmaline increased refractoriness over the accessory pathway, decreasing the mean ventricular rate of 300 beats/min to 160 beats/min. In two patients ajmaline was continued as an intravenous maintenance infusion until sinus rhythm was restored. It is concluded that ajmaline is an effective drug for the acute management of atrial flutter or fibrillation with a fast ventricular response in patients with the Wolff-Parkinson-White syndrome.

Terminal QRS distortion on admission is better than ST-segment measurements in predicting final infarct size and assessing the Potential effect of thrombolytic therapy in anterior wall acute myocardial infarction.

We assessed predicting final infarct size (using predischarge Selvester score) by 3 electrocardiographic variables in 267 patients with first anterior wall acute myocardial infarction (AMI) undergoing (n = 86) or not undergoing (n = 181) thrombolysis. Patients with previous AMI or inverted T waves in leads with ST elevation were excluded. The sum (sigma) of ST elevation, the number of leads with ST elevation, and the initial electrocardiographic pattern were determined on the admission electrocardiogram (absence (QRS-) or presence (QRS+) of distortion of the terminal portion of the QRS in > or =2 leads (J point > or =0.5 of the R-wave amplitude in leads I, aVL, V4 to V6, or presence of ST elevation without S waves in leads V1 to V3). There was no association between sigmaST elevation and final infarct size in patients who did or did not receive thrombolytic therapy. Analysis of covariance showed that the number of leads with ST elevation (F = 19.6), thrombolysis (F = 25.2), and QRS+ initial pattern (F = 19.5) were all associated with final infarct size (p <0.0001 for all). Among patients who did not receive thrombolytic therapy, the average Selvester score was 19.7+/-9.9 for the QRS- patients and 26.1+/-10.4 for the QRS+ patients (p = 0.02). Among patients who received thrombolytic therapy, the average Selvester score was 11.7+/-9.8 for the QRS- patients and 24.2+/-10.1 for the QRS+ patients (p <0.0001). Thrombolysis reduced final Selvester score only in the QRS- group (p <0.00001), but not in the QRS+ group (p = 0.45). It is concluded that (1) final Selvester score in anterior wall AMI can be predicted by the number of leads with ST elevation, the initial electrocardiographic pattern, and thrombolysis, and (2) thrombolysis reduces final Selvester score only in patients with QRS- pattern.

Multiform accelerated idioventricular rhythm in acute myocardial infarction: electrocardiographic characteristics and response to verapamil.

Thirteen patients with acute myocardial infarction with multiform accelerated idioventricular rhythm (AIVR) occurring during the first 12 hours of monitoring in the coronary care unit are described. This arrhythmia, similar to the more common uniform AIVR, was intermittent, did not cause hemodynamic compromise, and was not related to more serious ventricular arrhythmias. There was no correlation between the bundle branch block pattern of the multiform AIVR and the electrocardiographic location of the myocardial infarction, but there was a perfect correlation between the frontal plane electrical axis of the multiform AIVR and the electrocardiographic location of the myocardial infarction. The presence of fusion beats between the different forms of AIVR suggests multifocality rather than multiformity. Intravenous verapamil (3 to 5 mg bolus) was administered to 6 patients with multiform AIVR in whom the arrhythmias were persistent enough to allow the evaluation of the effect of verapamil on the arrhythmia. Verapamil caused no change in the rate of AIVR in 1 patient, but in a second patient it decreased the rate by 20 beats/min. In 4 patients, verapamil abolished the arrhythmia: in 2 patients carotid sinus pressure (induced sinus slowing) allowed the emergence of the AIVR at a lower rate, and in the remaining 2 patients the arrhythmia was not observed.