Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.     

A patient in whom self-terminating ventricular fibrillation was a manifestation of myocardial reperfusion

Self-terminating ventricular fibrillation was recorded in a 47 year old woman without coronary artery or other structural heart disease. Reperfusion was thought to be responsible for the ventricular fibrillation because the arrhythmia started while the ST segment was returning to the baseline during an episode of silent ischaemia that was probably caused by coronary spasm. This case shows that potentially lethal arrhythmias can arise during reperfusion and that ventricular fibrillation during reperfusion may be self-terminating.     

5-HT1Dbeta receptor mediates the supersensitivity of isolated coronary artery to serotonin in variant angina

Although serotonin (5-hydroxytryptamine; 5-HT) is used for provocation of coronary spasm, 5-HT receptor subtypes in spastic coronary arteries remain undetermined. We demonstrated the supersensitivity of isolated coronary artery to ergonovine, 5-HT, and sumatriptan, a 5-HT1D receptor agonist, in a patient with variant angina. Furthermore, we detected gene expression of 5-HT1Dbeta and 5-HT2A receptors in spastic coronary artery using RNase protection assay. These findings suggest that the leftward shift of the dose-response curve for 5-HT, which plays an important role in the pathogenesis of coronary spasm, is mediated by activation of 5-HT1Dbeta receptor.     

Effective low-dose amiodarone therapy for ventricular tachycardia complicated with ischemic heart disease and poor left ventricular function in an elderly patient

A 71-year-old man who had ischemic heart disease with poor left ventricular function and ventricular tachycardia was admitted to hospital for evaluation. Cardiac catheterization was performed on August 19, 1996, and right coronary arteriography revealed total occlusion at segment 3. Left coronary arteriography revealed total occlusion at segment 6, and a lesion at segment 13 was 75% occluded. Partial collateral flow from the right ventricular branch to the left anterior descending artery was demonstrated, and the left ventricular ejection fraction was 24%. Recurrent ventricular tachycardia followed by pre-syncope occurred from August 23, 1996, and the patient underwent emergency coronary artery bypass surgery to the left anterior descending artery and circumflex artery using saphenous vein grafts. Ventricular tachycardia followed by pre-syncope occurred frequently after the bypass surgery, and antiarrhythmic agents (Vaughan Williams classification Ia and Ib groups) were ineffective. He received amiodarone (100 mg/day after a loading dose of 200 mg/day for 2 weeks) from September 6, 1996. His symptoms of arrhythmia decreased, and side effects have not been observed. Low-dose amiodarone was effective in this case of ischemic heart disease with left ventricular dysfunction and sustained ventricular tachycardia.     

Action of intracoronary nitroglycerin in refractory coronary artery spasm

Coronary artery spasm usually responds to sublingual nitroglycerin. This report describes four patients with variant angina and one patient with rest angina who had coronary spasm that was refractory to sublingual or i.v. nitroglycerin. In four patients, spasm occurred spontaneous and in one patient after 0.05 mg of ergonovine. In each case, 25-100 micrograms of intracoronary nitroglycerin promptly (30-45 seconds) resulted in reopacification of the vessel involved in spasm and resolution of evidence for ischemia. Thus, intracoronary nitroglycerin can reverse coronary artery spasm that does not respond to systemic nitroglycerin administration.     

Arrhythmogenic ventricular aneurysms unrelated to coronary artery disease

Malignant ventricular tachycardia occurs most frequently in patients with coronary artery disease who have had a previous myocardial infarction and in whom a ventricular aneurysm subsequently develops in the scarred section of myocardium. Ventricular tachycardia in the presence of normal coronary arteries and a left ventricular aneurysm is unusual and can be refractory to medical therapy. We retrospectively reviewed our experience of 10 patients treated at our institution from 1983 to 1993. Age ranged from 22 to 76 years, and all patients presented with sustained ventricular tachycardia. All patients underwent complete electrophysiologic testing. Cardiac catheterization was performed in 9 patients, and each had normal coronary artery anatomy without evidence of significant fixed lesions. A left ventricular aneurysm, diagnosed by either echocardiography, thoracic cine computed tomography or magnetic resonance imaging, or ventricular angiography was present in all patients. Ventricular tachycardia could not be suppressed pharmacologically in 7 of 10 patients using multiple agents including procainamide, quinidine, flecanide, tocainide, propaferone, and amiodarone. Six patients were treated surgically by intraoperative electrophysiologic mapping, endocardial resection of foci, and left ventricular aneurysmectomy. An implantable cardiac defibrillation device was implanted in 2 patients. One patient died on the second postoperative day after simultaneous mapping -guided aneurysmectomy and implantable cardioverter defibrillator placement. There was one late postoperative death. All other surgically treated patients had postoperative electrophysiologic studies demonstrating no inducible ventricular tachycardia, and these patients remain without antiarrhythmic therapy in follow-up extending from 29 to 86 months (mean, 56 months).(ABSTRACT TRUNCATED AT 250 WORDS)     

Inhibition of malaria-infected erythrocytes by deoxyspergualin: effect on in vitro growth of malarial cultures

The aim of this study was to assess whether the psychobehavioral pattern alexithymia is related to coronary artery spasm. Alexithymia, deficient psychological awareness, was examined using the Minnesota Multiphasic Personality Inventory Alexithymia Scale in 100 patients with angina pectoris in whom coronary spasm, defined as > or = 99% coronary narrowing, was documented upon ergonovine provocation, and in 109 patients with chest pain syndrome who were shown to have almost normal coronaries without inducible coronary spasm on coronary angiogram (control group). Alexithymia was approximately twice as prevalent in the coronary spasm group (31%) as in the control group (14%) (p<0.01). Among various conventional risk factors including hyperlipidemia, obesity, diabetes mellitus, hypertension, hyperuricemia, or family history of ischemic heart disease, only male sex and smoking were more prevalent in the coronary spasm group than in the control group (p<0.001). The odds ratios of coronary spasm adjusted for all the other risk parameters including sex and age were 4.14 [95% confidence interval (CI) 1.81-9.47] for alexithymia and 2.38 (95, CI 1.18-4.82) for smoking. A psychobehavioral pattern, alexithymia, relates to coronary spasm. This relationship is independent of the conventional coronary risk factors.     

Glycation mediated lens crystallin aggregation and cross-linking by various sugars and sugar phosphates in vitro

BACKGROUND: The role of coronary spasm in underlying disease-free patients who were resuscitated from sudden cardiac arrest remained uncertain. This study investigated the cause of cardiac arrest, and the etiologic and prognostic differences were compared between patients with underlying heart disease (group I) and those patients without underlying heart disease (group II). METHODS: Twenty-five survivors of sudden cardiac arrest were classified into two groups according to the presence or absence of underlying heart disease. To investigate the cause of cardiac arrest, we performed ergonovine testing and electrophysiologic study. Fifteen of the patients had underlying heart disease, while 10 did not. RESULTS: Electrophysiologic abnormalities were found in 13 of the 15 patients in group I. In group II, spontaneous attack of coronary spasm occurred in four patients during the observation period, and coronary spasm was induced in three of the remaining six period of 32 +/- 23 months, whereas no patients in group II had recurrence of sudden cardiac arrest at a median follow-up of 32 months (range, 10 to 72 months). CONCLUSIONS: Electrophysiologic study identified a potential cause in 13 of 15 patients with underlying heart disease. Coronary spasm was involved in the pathogenesis of sudden cardiac arrest in survivors without identifiable underlying heart disease.     

Analysis of reperfusion by thrombolysis of the artery responsible for acute myocardial infarction

OBJECTIVE: To analyze the role of the culprit coronary artery in myocardial infarction, its evolution and mortality. And to correlate with clinical criteria of reperfussion. MATERIALS AND METHODS: We included patients with clinical diagnosis of acute myocardial infarction (MI) treated with thrombolytic therapy, and coronariography. We used the TIMI study angiographic scale to evaluate the level of permeability of the culprit artery. RESULTS: Of 473 patients with of acute MI; coronariography was made in 377. The most frequent culprit vessel was anterior descending artery in 168 patients (45%) and right coronary artery in 139 patients (36%). In 276 patients the culprit vessel was permeable (73%). Of them in 30 patients, had TIMI 1 alterations, TIMI 2 in 97 patients, had TIMI 3 in 148 patients, only 102 patients had TIMI 0. In anterior MI the most frequent reperfussion arrhythmia was ventricular ectopic beats followed by slow ventricular tachycardia and ventricular tachycardia in 54%, ventricular fibrillation was observed only in six patients, of whom TIMI scale was 2 and 3 in five patients. In inferior MI, ventricular ectopic beats and slow ventricular tachycardia was seen in 25% of patients. In patients with permeable culprit artery we observed significant depression of ST segment, (159 patients, 42%), and significant increase in CK-MB levels, seen in 191 patients (51%). In the group of patients with total occlusion of the culprit artery, twenty-one (30%) had left ventricular disfuntion, and only six of them were in cardiogenic shock. In the group of patients with permeable culprit artery only two percent had cardiogenic shock. Therefore the analysis of the clinical evolution is the maia marker to take into consideration to send patients to early coronary arteriography with the objective to look for other therapeutic alternatives.     

Results and efficiency of programmed ventricular stimulation with four extrastimuli compared with one, two, and three extrastimuli

BACKGROUND: Conventional programmed ventricular stimulation protocols are inefficient compared with more recently proposed protocols. The purpose of the present study was to determine if additional efficiency could be derived from a 6-step programmed ventricular stimulation protocol that exclusively uses four extrastimuli. METHODS AND RESULTS: The subjects were 209 consecutive patients with coronary artery disease and documented sustained monomorphic ventricular tachycardia, nonsustained ventricular tachycardia, aborted sudden death, or syncope. These patients underwent 159 electrophysiological tests in the absence of antiarrhythmic drug therapy and 105 electrophysiological tests in the presence of antiarrhythmic therapy. Programmed stimulation was performed with two protocols in random order in each patient. Both protocols used an eight-beat drive train, 4-s intertrain pause, and basic drive cycle lengths of 350, 400, and 600 ms. The 6-step protocol started with coupling intervals of 290, 280, 270, and 260 ms, which were shortened simultaneously in 10-ms steps until S2 was refractory. The 18-step protocol used one, two and three extrastimuli in conventional sequential fashion. The end points were 30 s of sustained monomorphic ventricular tachycardia, two episodes of polymorphic ventricular tachycardia requiring cardioversion, or completion of the protocol at two right ventricular sites. There was no significant difference in the yield of sustained monomorphic ventricular tachycardia using the two protocols, regardless of the clinical presentation or treatment with antiarrhythmic drugs. Polymorphic ventricular tachycardia occurred with the 18-step protocol twice as frequently as with the 6-step protocol (6% versus 3%, P < .001). The duration of the 18-step protocol was significantly longer than that of the 6-step protocol in patients with inducible ventricular tachycardia (5.5 +/- 7 versus 2.3 +/- 2 minutes, P < .001), as well as in patients without inducible ventricular tachycardia (25.4 +/- 7 versus 6.9 +/- 2 minutes, P < .001). CONCLUSION: A stimulation protocol that exclusively uses four extrastimuli improves the specificity and efficiency of programmed ventricular stimulation without compromising the yield of monomorphic ventricular tachycardia in patients with coronary artery disease.     

Coronary vasoreactivity to ergonovine after angioplasty: difference between the infarct-related coronary artery and the noninfarct-related coronary artery

BACKGROUND: The vasoreactivity after direct percutaneous transluminal coronary angioplasty (PTCA) in patients with previous myocardial infarction remains unknown. We examined the constrictor response to ergonovine of the infarct-related coronary artery in comparison with that of noninfarct-related coronary artery after angioplasty. METHODS: Ergonovine was administered intravenously to 17 patients with previous myocardial infarction (group I) and to 21 patients with stable angina (group II) 1 year after PTCA. The effects of ergonovine on lumen diameter were analysed quantitatively at the PTCA segment, nonPTCA segment (proximal to the PTCA segment), and nonPTCA artery. RESULTS: The ergonovine-induced decrease in minimal lumen diameter at the PTCA segment was significant in group I (decrease from 2.12 +/- 0.56 to 1.39 +/- 0.74 mm, P < 0.01), but not in group II (decrease from 1.60 +/- 0.35 to 1.43 +/- 0.33 mm, NS). Patients in group I showed a constrictor response at the nonPTCA artery (decrease in diameter from 2.54 +/- 0.90 to 1.94 +/- 0.77 mm, P < 0.01), and a tendency to constrict at the nonPTCA segment (2.56 +/- 0.67 to 2.11 +/- 0.66 mm, P = 0.06), whereas those in group II showed no significant constrictor response to ergonovine at any of the three segments examined. The changes in diameter at the three segments in patients in group I were significantly greater than those in group II (all P < 0.01). Subtotal coronary spasm at the PTCA segment was provoked only in three patients in group I (18%). CONCLUSIONS: The constrictor response to ergonovine of the infarct-related coronary artery was enhanced compared with that of the noninfarct-related coronary artery. This difference in coronary vasoreactivity at the angioplasty segment may be due to previous hypersensitivity of the smooth muscle.     

Dental fear with and without blood-injection fear: implications for dental health and clinical practice

BACKGROUND: It has been suggested that the sympathetic nervous system might play an important role in the development of coronary artery spasm. However, no cardiac imaging modality has been able to demonstrate abnormal sympathetic innervation in patients with coronary artery spasm. The purpose of this study was to assess the presence and location of abnormal sympathetic innervation using iodine 123-metaiodobenzylguanidine (123I-MIBG) single photon emission computed tomography (SPECT) and to evaluate the clinical efficacy of 123I-MIBG SPECT as a noninvasive screening test in patients with coronary artery spasm. METHODS AND RESULTS: Coronary arteriography and a provocative test with intravenous administration of ergonovine maleate were performed in 26 patients (20 men, 6 women, mean age 48.2+/-12.0 years, range 20 to 67 years) who were suspected of having a coronary artery spasm. The subjects were divided into 2 groups: group 1 (n = 18) comprised subjects with a positive provocative test result, and group 2 (n = 8) comprised subjects with negative provocative test results. Ten healthy subjects served as controls. No abnormal MIBG uptake was observed in the control subjects. Abnormal sympathetic nervous innervation using 123I-MIBG SPECT was observed either as a reduced uptake or a defective pattern in the perfused areas in 13 of the 18 regions supplied by vessels of ergonovine-induced vasospasm. Normal sympathetic innervation, as evidenced by normal 123I-MIBG uptake, was noted in all of the 60 segments of normal vessel territories. Reduced uptake of 123I-MIBG was not detected in the perfused areas of 5 vasospasm-induced vessels (perfusion territory of left anterior descending coronary artery [LAD] and the right coronary artery [RCA] in 2 and 3 patients, respectively). The sensitivity and specificity of 123I-MIBG for detection of coronary artery spasm were 72.2% (95% confidence interval [CI] 55% to 89%) and 100%, respectively. The positive predictive and negative predictive values were 100% and 92.3% (95% CI 91% to 93%), respectively. CONCLUSION: 123I-MIBG SPECT is a feasible method to evaluate noninvasively and localize the territories of coronary arteries with spasm. Invasive diagnostic coronary arteriography with ergonovine provocation test may be unnecessary for diagnosis of coronary artery spasm in patients with typical resting pain, negative exercise test or normal thallium perfusion scan results, but showing abnormalities in 123I-MIBG SPECT.     

Re-examination of the mutagenicity of ethylene glycol monobutyl ether to Salmonella tester strain TA97a

Widespread use of implantable cardioverter defibrillators (ICDs) for the treatment of ventricular tachycardia (VT) and ventricular fibrillation (VF) occurred in the late 1980s and early 1990s. Additionally, there has been increasing appreciation during this time for both the lack of efficacy and proarrhythmic activity of antiarrhythmic drugs to treat these cardiac arrhythmias. We evaluated the use of antiarrhythmic drugs from 1987 to 1991 (5-year period) at the time of ICD implantation in 25,450 patients. The use of all classes of antiarrhythmic agents decreased from 61% to 24% during this time period (P < 0.05). In addition, there was a significant reduction in antiarrhythmic agent use for each drug class (P < 0.05) with the exception of Class II agents (beta blockers). These changes in drug use occurred independent of any changes in age, sex, ejection fraction, prevalence of coronary artery disease, or type of ventricular arrhythmia (VT vs VF).     

Ergonovine-echo test to assess the significance of chest pain at rest without ECG changes

The aim of this study was to assess the feasibility and diagnostic role of ergonovine maleate infusion under continuous two-dimensional echocardiographic monitoring for the identification of vasospastic myocardial ischaemia in patients with chest pain at rest not associated with diagnostic ECG changes. One hundred and twenty-eight consecutive patients, selected on the basis of absence of ischaemic ECG changes during angina at rest before or during hospitalization, were enrolled in the study. Ergonovine maleate was i.v. administered in scaled doses (from 0.025 to 0.2 mg at 10 min intervals) under echocardiographic, electrocardiographic and systemic blood pressure monitoring. Wall motion asynergies were observed in 33 patients, accompanied by typical chest pain in 24 patients and by ECG changes in 25 (ST elevation in 13 patients, ST depression in seven, T wave changes in five). All patients were able to complete the test. Non life-threatening ventricular arrhythmias were observed in four patients exclusively in association with ischaemia. In seven patients with a positive test, coronary artery spasm was documented at angiography. In 16 patients with a positive test, the vasospastic event was reproduced by a hyperventilation-echo test or a second ergonovine maleate-echo test performed within 3 days of the first examination. In none of the patients with a negative test was documentation of myocardial ischaemia due to a primary reduction in coronary blood flow. Thus, in patients who do not show ECG changes during chest pain at rest, the ergonovine maleate-echo test is feasible and safe; it permits the recognition of ischaemic episodes on the basis of wall motion abnormalities when conventional 12-lead ECG-recorded chest pain is non-diagnostic.     

Long-term efficacy of d/l sotalol in patients with sustained ventricular tachycardia refractory to class I antiarrhythmic drugs

The efficacy of d/l sotalol was investigated in 50 patients (43 men, seven women; 33 with coronary artery disease, 15 with dilated cardiomyopathy; ejection fraction 33 +/- 10%) with inducible sustained ventricular tachycardia. Before d/l sotalol a mean of 2 +/- 1 (1 to 4) class I antiarrhythmic drugs were ineffective. In 24 patients (48%) oral d/l sotalol (320 +/- 47 mg.day-1) prevented induction of the ventricular tachycardia; in 23 patients the ventricular tachycardia remained inducible (d/l sotalol 326 +/- 50 mg.day-1). The electrophysiological effects of d/l sotalol did not differ between patients in whom d/l sotalol prevented induction of ventricular tachycardia and those in whom the ventricular tachycardia remained inducible. In two patients, torsade des pointes developed after oral application of d/l sotalol; one patient suffered from severe hypotension even with 80 mg of sotalol per day. During long-term follow-up (27 +/- 12 months) 5/24 patients (21%) had a non-fatal recurrence of ventricular tachycardia (1 week to 21 months), one patient died suddenly and another from progressive heart failure. In patients in whom the ventricular tachycardia could be induced despite oral application of d/l sotalol, control of the ventricular tachyarrhythmia was attempted by the use of sotalol in combination with mexiletine (n = 2), amiodarone (n = 9), catheter ablation (n = 2), antitachycardia surgery (n = 1) or the implantation of an automatic cardioverter defibrillator (n = 12). Recurrence of ventricular tachycardia was observed in four patients without an implanted cardioverter defibrillator. Seven out of 12 patients with an implanted cardioverter defibrillator received appropriate shocks or successful antitachycardia pacing. Although no patient died suddenly, overall mortality was 17% in this group. It is concluded that d/l sotalol is highly effective in the suppression of sustained monomorphic ventricular tachycardia inducible by programmed electrical stimulation. However during a mean follow-up of 27 +/- 12 months a recurrence of ventricular tachycardia was seen in 21% of patients, and one patient died suddenly.     

Importance of abortive shock capability with electrogram storage in cardioverter-defibrillator devices

OBJECTIVES: This study evaluates the ability of a third-generation cardioverter-defibrillator to abort energy delivery and the importance of electrogram storage in analyzing the aborted events. BACKGROUND: In the Cadence Tiered Therapy Defibrillator, when a tachycardia satisfies detection criteria for cardioversion or defibrillation therapy, high voltage capacitors begin charging. The Cadence defibrillator continues monitoring the rhythm during charging and if the rate decreases to below the rate triggering therapy, charging is terminated. This event is registered as an aborted shock. The defibrillator also has the ability to store intracardiac electrogram recordings of the electrical events that precipitate device therapy or aborted shocks. METHODS: During a mean follow-up interval of 10 +/- 7 months, 55 aborted events were registered by the Cadence defibrillator in 18 of the 49 patients who received it. Thirty-two stored ventricular electrograms of events leading to aborted shocks were available for analysis in 15 patients. RESULTS: Intracardiac electrogram recordings demonstrated the probable electrical events leading to these aborted shocks included nonsustained ventricular tachycardia (n = 10), nonsustained rapid polymorphic ventricular tachycardia/ventricular fibrillation (n = 2), atrial fibrillation (n = 5), supraventricular tachycardia (n = 2) and electrical noise (n = 13). Eleven patients had a therapeutic intervention initiated as a consequence of the diagnostic information provided by analysis of intracardiac electrogram recordings. Four of the 15 patients had no changes made. During a follow-up period of 9 +/- 5 months after therapy was altered, no patient had subsequent aborted shocks. Five patients have had seven appropriate shocks for sustained ventricular tachycardias. CONCLUSIONS: The ability of Cadence defibrillator to continue tachycardia sensing during capacitor charging and to abort shock therapy for self-terminating events prevented unnecessary shocks in 18 (37%) of the 49 patients. Intracardiac electrogram recordings were critical for instituting appropriate therapy that may have prevented unnecessary device charging and inappropriate discharges.     

Incidence and significance of ventricular tachycardia and fibrillation in the absence of hypotension or heart failure in acute myocardial infarction treated with recombinant tissue-type plasminogen activator: results from the Thrombolysis in Myocardial Infarction (TIMI) Phase II trial

OBJECTIVES: The purpose of this study was to determine the incidence of ventricular tachycardia and fibrillation without hypotension or heart failure after treatment with recombinant tissue-type plasminogen activator (rt-PA), anatomic correlates of their development, the effect of immediate intravenous metoprolol on their occurrence and the outcome of patients with these arrhythmias. BACKGROUND: Malignant arrhythmias after thrombolytic therapy have been reported to occur as a result of coronary reperfusion, which is associated with reduced mortality in patients receiving thrombolytic therapy. METHODS: We analyzed data from 2,546 patients in the Thrombolysis in Myocardial Infarction (TIMI) Phase II trial without congestive heart failure or hypotension during the 1st 24 h after study entry. Forty-nine patients (1.9%) developed sustained ventricular tachycardia or ventricular fibrillation within 24 h of study entry (group 1), and 2,497 patients (98.1%) did not (group 2). RESULTS: Baseline characteristics and admission laboratory values were similar in the two groups. In patients undergoing protocol angiography 18 to 48 h after rt-PA, the infarct-related artery was patient in a greater percent of group 2 patients (87% [1,015 of 1,169]) than group 1 patients (68% [15 of 22], p = 0.01), although angiography was performed less frequently in group 1 than in group 2. More group 1 than group 2 patients died within 21 days (20.4%) (1.6%, p < 0.001). For patients surviving to 21 days, there was no difference in mortality between patients in the two groups in the following year. CONCLUSIONS: Ventricular tachycardia and fibrillation are not markers for reperfusion after thrombolytic therapy. These arrhythmias are associated with occlusion, not patency, of the infarct-related artery. Early mortality is increased in patients who develop ventricular tachycardia and fibrillation, even in the absence of congestive heart failure and hypotension.     

Unexpected instant death following successful coronary artery bypass graft surgery (and other clinical settings): atrial fibrillation, quinidine, procainamide, et cetera, and instant death

Primum non nocere. Atrial fibrillation (AF) occurs commonly following coronary artery bypass graft surgery, although new onset atrial fibrillation in this setting is usually transient. When AF reverts or is converted to sinus rhythm it is unlikely to recur, whether or not the patient takes preventive medication. As no benefit (and sometimes increased risk) associated with reduced mortality or morbidity in this setting has been reported for antiarrhythmic agents, standard treatment should consist of observation or control of ventricular response with an appropriate agent until AF relapses to sinus rhythm. If an antiarrhythmic agent, especially a class I agent, is used because of persistent or recurrent AF in the early postoperative period, heart rhythm should be monitored as long as the class I agent is administered and treatment initiated if an undersirable rhythm develops. Atrial fibrillation in other clinical settings in patients with structural heart disease presents a more difficult management problem. Class I agents are reported to be associated with an increased risk of death, despite an efficacious effect of maintaining sinus rhythm. Amiodarone is reported to be well tolerated with respect to the cardiovascular system, but unacceptable noncardiac effects are reported. A safe amiodarone-like agent is greatly needed. Atrial fibrillation in patients with no structural heart disease is not discussed in this presentation.     

Selective ergonovine-induced coronary artery spasm and ST-segment alternans after blunt thoracic trauma

A 24-year-old man was found to have angiographically normal coronary arteries shortly after suffering blunt thoracic trauma. Selective ergonovine administration into the left coronary artery induced total occlusion of the left anterior descending branch and electrical alternans of the ST-segment. This case demonstrates coronary artery spasm as a possible mechanism of coronary occlusion after blunt thoracic trauma.     

Evaluation of antiarrhythmic efficacy of sotalol in various doses in patients with ventricular tachyarrhythmias

Antiarrhythmic efficacy of sotalol--noncardioselective beta-adrenergic blocking agent with class III antiarrhythmic action was evaluated in 34 patients [pts] (mean age 55 +/- 11) with chronic ventricular arrhythmias and coronary artery disease, 38% with previous myocardial infarction. Two schedules of dosing were tested: 3 x 80 mg and 2 x 160 mg during 28 days of therapy. Pts with Lown class II and IV arrhythmia derived from 24-hours Holter recording were assigned. Ventricular premature complexes [VPCs] and couplets reduction by 80% and total elimination of runs defined antiarrhythmic efficacy. Proarrhythmia was defined by four times increase in VPCs, ten times increase in couplets and runs or sustained VT episodes. RESULTS: Antiarrhythmic efficacy of two doses of sotalol according to study criterion was: 31% for lower dose (3 x 80 mg) and 24% for higher dose (2 x 160 mg). Overall efficacy for both doses was 55%. According to Morganroth criterion, lower dose was effective in 29% pts and both doses, lower and higher, in 41% pts. According to other commonly used criterion: 70% VPCs reduction, 90% couplets reduction and total elimination of runs, lower dose of sotalol was effective in 32% pts and both doses in 47% pts. Significant reduction of heart rate and prolongation of QT and QTc were observed. In 3 pts QT was prolonged over 500 ms. Proarrhythmia according to Velebit criterion was suspected in one patient after one week of 3 x 80 mg teratment which caused premature cessation of therapy. No significant abnormalities in laboratory values were observed. CONCLUSIONS: Antiarrhythmic efficacy of sotalol was comparable to other studies. Its value in pts with malignant ventricular tachyarrhythmias: sustained ventricular tachycardia and ventricular fibrillation requires further studies with higher number of patients.