Quantitating AV nodal function: has A1A2 outlived its usefulness?
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Biomedical subjects
Publications and source records attributed to M D Meissner.
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A broad array of therapeutic options is currently available for the management of patients with AV nodal reentrant tachycardia. While acute termination of tachycardias is readily achieved, either by vagal maneuvers or intravenous medication, the decision to embark on a long-term therapeutic plan to prevent recurrences must be clinically individualized. When a chronic pharmacologic approach is desired, electrophysiologic testing is invaluable for confirming the diagnosis and selecting appropriate medication. However, the growing awareness of potential proarrhythmic effects and the inconvenience and expense of lifelong drug therapy, coupled with other advances in the field, have made nonpharmacologic approaches more attractive. This is especially so for symptomatic younger patients. The definitive cure rates achievable with surgery are now being approached by transcatheter AV nodal modification procedures that ablate AV nodal reentrant tachycardia while preserving anterograde AV nodal conduction. Over the next decade, it is likely that the latter technique will become widely used for the long-term management of symptomatic AV nodal reentrant tachycardia.
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This study assessed the relation between acute antiarrhythmic drug efficacy and left ventricular (LV) function in patients with sustained ventricular tachyarrhythmias, that is, sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Electrophysiologic studies (n = 560) were performed in 201 patients, separated for analysis into less than 30 and greater than or equal to 30% ejection fraction groups. Coronary artery disease was present in all patients. The 8 acute antiarrhythmic regimens were procainamide, quinidine, mexiletine, mexiletine + type 1A agent, flecainide or indecainide, amiodarone, amiodarone + type 1A and "miscellaneous" agents. At least 1 successful acute antiarrhythmic regimen was found in 47% of patients and in a significantly greater proportion of patients with ejection fraction greater than or equal to 30% (52 of 81 = 64%) than in those with ejection fraction less than 30% (43 of 120 = 36%, p less than 0.001). Drug trials were successful (initiation of less than 15 repetitive ventricular responses) in 32% of patients with ejection fraction greater than or equal to 30% versus 19% of those with ejection fraction less than 30% (p less than 0.001). There were no statistically significant differences between the 2 ejection fraction groups in type of heart disease, acute antiarrhythmic dosages or mean serum drug levels. A logistic regression analysis incorporating multiple clinically relevant factors found that ejection fraction was the only factor that correlated significantly with drug success or failure (p less than 0.002). Acute antiarrhythmic drug efficacy relates to LV function per se or to other pathophysiologic mechanisms of which ejection fraction may be a marker.
We used exercise thallium 201 imaging in 123 patients with diabetes mellitus (77 men and 46 women, aged 56 +/- 8 years), 75% of whom had angina pectoris (typical or atypical). During exercise testing, 18 patients (15%) had angina pectoris, 28 (23%) had ischemic ST changes, and 69 (56%) had abnormal thallium images. During follow-up (up to 36 months), there were 12 cardiac events; four patients died of cardiac causes and eight had nonfatal acute myocardial infarction. Univariate and multivariate survival analysis identified two independent predictors of cardiac events: the event rate was significantly less in patients with normal images and exercise heart rate over 120 beats per minute than in patients with abnormal images and exercise heart rate of 120 beats per minute or less (0% vs 22%). The patients with abnormal images or exercise heart rate of 120 beats per minute or less had an intermediate event rate (11.5%). Furthermore, two of the 54 patients with normal images and ten of 69 patients with abnormal images had subsequent cardiac events. Thus, exercise thallium imaging is useful in risk stratification in patients with diabetes mellitus.
This study assessed the determinants of exercise-induced abnormal systolic blood pressure (BP) response in 127 patients with documented coronary artery disease (CAD) who underwent exercise thallium-201 scintigraphy. Three types of systolic BP response to exercise were identified: an increase by more than 20 mm Hg (group I, n = 74); an increase by 20 mm Hg or less (group II, n = 36); and a decrease of at least 10 mm Hg (group III, n = 17). The 3 groups were not significantly different in age, gender or medications. The number of segments with perfusion defects was significantly higher in groups II and III than group I (group III, 2.9 +/- 1.5; group II, 2.9 +/- 2.1; and group I, 1.8 +/- 1.4, p = 0.009). Prior myocardial infarction, abnormal left ventricular ejection fraction, and multivessel CAD were more common in group III than in groups I and II. Stepwise discriminant analysis of 15 relevant clinical, angiographic and exercise scintigraphic descriptors showed that the number of thallium perfusion defects, abnormal LV ejection fraction at rest and multivessel CAD to be important predictors of hypotensive BP response. Multivariate analysis, however, showed that the number of thallium perfusion defects was the only important predictor of the hypotensive response. Thus, it is the functional significance of CAD assessed by the extent of thallium perfusion abnormalities rather than the extent of CAD or left ventricular dysfunction at rest that determines the systolic BP response to exercise.
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Ventricular tachyarrhythmia is the most common terminal event causing sudden cardiac death. Risk stratification using 24-hour Holter monitoring to identify ventricular ectopy and noninvasive techniques to detect abnormal left ventricular function is becoming routine. Many cardiologists treat patients with potentially lethal ventricular arrhythmias even though it is unknown as yet whether sudden cardiac death can be prevented. Patients with lethal ventricular arrhythmias are always treated. A number of new oral antiarrhythmic agents have become available to the clinician. The modified Vaughan-Williams classification system categorizes the drugs according to their electrophysiologic and clinical characteristics. The class IC antiarrhythmic agents are emerging as the potential drugs of first choice for patients with benign or potentially lethal ventricular arrhythmias. The betablockers (class II) are used as antiarrhythmic agents, particularly in the presence of active myocardial ischemia or high catecholamine levels and in the postmyocardial infarction patient. Amiodarone (class III) may cause serious side effects and is reserved for patients with lethal ventricular arrhythmias when all other available agents have failed.
Sudden death, a major cause of mortality in the Western world, usually results from electrophysiologic phenomena in chronically damaged hearts with advanced coronary atherosclerosis. The exact pathophysiologic mechanisms are not known, but there is reasonable circumstantial evidence to implicate myocardial ischemia--clinically manifest or silent--as one of probably multiple factors of pathogenetic significance. This may be on the basis of coronary artery spasm, platelet aggregation, left ventricular dysfunction perpetuating a vicious circle of hypoperfusion and ventricular vulnerability to electrical instability. The increasing use and quality of continuous ambulatory electrocardiographic (Holter) monitoring have allowed improved detection of ST-segment changes and arrhythmias. The majority of sudden deaths result from ventricular tachyarrhythmias degenerating into ventricular fibrillation, and a more significant proportion of these than had been previously thought may be ischemically mediated. Importantly, as many as 20 to 25 per cent of the approximately 450,000 yearly terminal events represent bradyarrhythmias that may be preceded or accompanied by silent myocardial ischemia. Research is still required to determine the incidence, role, and mechanisms of silent myocardial ischemia in sudden death, with the hope that this common catastrophic event can be better prevented.
The prognostic implications of coronary collateral channels were examined in 359 medically treated patients with one vessel coronary artery disease and a normal left ventricular ejection fraction (greater than or equal to 50%). There were 149 patients with isolated left anterior descending coronary artery disease (group I) and 210 patients with isolated left circumflex or right coronary artery disease (group II). Collateral channels were present in 68 patients (46%) in group I and 115 patients (55%) in group II. During a follow-up period of up to 82 months (mean +/- SD 34 +/- 18), there were 23 cardiac events (4 patients died of cardiac causes and 19 patients had a nonfatal acute myocardial infarction). Actuarial survival analysis showed that the risk of cardiac events was not related to the presence of collateral channels in the two groups. Thus, the risk of cardiac events is not related to the presence or absence of collateral channels in patients with one vessel coronary artery disease. Further, the risks of cardiac death (0.3%/yr) and nonfatal myocardial infarction (1.9%/yr) are very low in medically treated patients with one vessel coronary artery disease and a normal left ventricular ejection fraction.