Intermittent pacemaker dysfunction caused by digital mobile telephones.

OBJECTIVES: This study was designed to evaluate possible interactions between digital mobile telephones and implanted pacemakers. BACKGROUND: Electromagnetic fields may interfere with normal pacemaker function. Development of bipolar sensing leads and modern noise filtering techniques have lessened this problem. However, it remains unclear whether these features also protect from high frequency noise arising from digital cellular phones. METHODS: In 39 patients with an implanted pacemaker (14 dual-chamber [DDD], 8 atrial-synchronized ventricular-inhibited [VDD(R)] and 17 ventricular-inhibited [VVI(R)] pacemakers), four mobile phones with different levels of power output (2 and 8 W) were tested in the standby, dialing and operating mode. During continuous electrocardiographic monitoring, 672 tests were performed in each mode with the phones positioned over the pulse generator, the atrial and the ventricular electrode tip. The tests were carried out at different sensitivity settings and, where possible, in the unipolar and bipolar pacing modes as well. RESULTS: In 7 (18%) of 39 patients, a reproducible interference was induced during 26 (3.9%) of 672 tests with the operating phones in close proximity (<10 cm) to the pacemaker. In 22 dual-chamber (14 DDD, 8 VDD) pacemakers, atrial triggering occurred in 7 (2.8%) of 248 and ventricular inhibition in 5 (2.8%) of 176 tests. In 17 VVI(R) systems, pacemaker inhibition was induced in 14 (5.6%) of 248 tests. Interference was more likely to occur at higher power output of the phone and at maximal sensitivity of the pacemakers (maximal vs. nominal sensitivity, 6% vs. 1.8% positive test results, p = 0.009). When the bipolar and unipolar pacing modes were compared in the same patients, ventricular inhibition was induced only in the unipolar mode (12.5% positive test results, p = 0.0003). CONCLUSION: Digital mobile phones in close proximity to implanted pacemakers may cause intermittent pacemaker dysfunction with inappropriate ventricular tracking and potentially dangerous pacemaker inhibition.

Important differences between short- and long-term hemodynamic effects of amiodarone in patients with chronic ischemic heart disease at rest and during ischemia-induced left ventricular dysfunction.

To assess and compare the hemodynamic profile of short-and long-term amiodarone administration in the same set of patients and to investigate hemodynamic mechanisms responsible for the antianginal effect of this drug, 10 patients with documented coronary artery disease and stable angina pectoris were studied. Simultaneous right heart catheterization and equilibrium radionuclide angiocardiography were performed at rest and during exercise before therapy (control), after a 5 minute intravenous infusion of 7.5 mg/kg of amiodarone and after 21.0 +/- 4.3 days of peroral therapy (10 days 800 mg/day, 7 days 400 mg/day and then 200 mg/day). After acute drug administration, ejection fraction, stroke index and systolic blood pressure decreased, whereas heart rate, left and right ventricular filling pressures and systemic vascular resistance increased. These effects were reversed after long-term therapy; all measured values returned to control levels except for heart rate, which decreased below the control value, and right atrial pressure, which remained slightly elevated. Amiodarone drug levels decreased from 4.8 +/- 1.8 after intravenous infusion to 1.2 +/- 0.6 mg/liter after long-term therapy. After adjustment for hemodynamic changes at rest, there were still significant reductions in heart rate, mean arterial pressure and rate-pressure product during exercise. It is concluded that the marked negative inotropic effect of amiodarone administered acutely in the dose applied calls for cautious use of this drug when administered intravenously. In contrast, long-term oral amiodarone therapy seems hemodynamically safe, even in patients with moderately depressed left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Silent ischemia after percutaneous transluminal coronary angioplasty: incidence and prognostic significance.

OBJECTIVES: The objective of this observational study was to assess the incidence and prognostic significance of silent ischemia after percutaneous transluminal coronary angioplasty. BACKGROUND: Apart from coronary angioplasty, prognosis of patients with silent ischemia is similar to that of patients with angina pectoris. However, similar data concerning silent ischemia associated with restenosis after coronary angioplasty are missing. METHODS: A consecutive series of 490 patients was investigated for asymptomatic ischemia on thallium-201 scintigraphy 6 months after successful coronary angioplasty. Repeat angiography was performed in a subgroup of patients with ischemia and repeat angioplasty was performed when clinically indicated. Patients were followed up for 2.2 +/- 0.8 years for cardiac events. RESULTS: Six months after coronary angioplasty, ischemia was present in 112 (28%) of 405 patients, and 60% of these 112 were asymptomatic. Ischemia was associated with significant stenosis in 97%; in contrast, results of exercise electrocardiography were negative in 74% of patients with scintigraphic ischemia and angiographic restenosis. The degree of restenosis was similar in patients with symptomatic or silent ischemia (80 +/- 16% vs. 81 +/- 21%). The long-term prognosis of patients with silent ischemia was remarkably similar to that of symptomatic patients. A worse outcome of symptomatic patients was found only if repeat coronary angioplasty for restenosis was considered a separate event (p < 0.01). Silent and symptomatic ischemia predicted an increased risk for recurrent ischemic events but not for death. CONCLUSIONS: Thus, absence of symptoms and negative findings on an exercise electrocardiogram may not reflect a good angioplasty result. In addition, silent ischemia due to restenosis after coronary angioplasty has a significant prognostic importance for recurrent symptomatic ischemic events that may be reduced by repeat angioplasty.

Effect of antiarrhythmic therapy on mortality in survivors of myocardial infarction with asymptomatic complex ventricular arrhythmias: Basel Antiarrhythmic Study of Infarct Survival (BASIS)

In view of the high risk of sudden cardiac death and the prognostic importance of complex ventricular ectopic activity, the effects of prophylactic antiarrhythmic treatment were investigated prospectively in patients with persisting asymptomatic complex arrhythmias after myocardial infarction. End points were total mortality and arrhythmic events (sudden death, sustained ventricular tachycardia and ventricular fibrillation). Of 1,220 consecutively screened survivors of myocardial infarction, 312 had Lown class 3 or 4b arrhythmia on 24 h electrocardiographic recordings before hospital discharge and consented to the study. They were randomized to individualized antiarrhythmic treatment (Group 1, n = 100), treatment with low dose amiodarone, 200 mg/day (Group 2, n = 98) or no antiarrhythmic therapy (Group 3 [control group], n = 114). During the 1 year follow-up period, 10 patients in Group 1 died, as did 5 in Group 2 and 15 in Group 3. On the basis of an intention to treat analysis, the probability of survival of patients given amiodarone was significantly greater than that of control patients (p less than 0.05). In addition, arrhythmic events were significantly reduced by amiodarone (p less than 0.01). These effects were less marked and not significant for individually treated patients (Group 1). These findings suggest that low dose amiodarone decreases mortality in the 1st year after myocardial infarction in patients at high risk of sudden death.

Time dependence of left ventricular recovery after delayed recanalization of an occluded infarct-related coronary artery: findings of a pilot study.

OBJECTIVES: We sought to test the hypothesis that late recanalization of infarct-related coronary arteries (IRAs) improves long-term left ventricular (LV) function. BACKGROUND: Reperfusion within 24 h of an acute myocardial infarction (MI) has been shown to improve myocardial healing and to reduce infarct expansion. Uncontrolled data suggest that there may be a time window of several weeks for such an effect. METHODS: Sixteen asymptomatic patients 10 +/- 4 days after a first Q wave anterior wall MI with persistent left anterior descending coronary artery occlusion and infarct-zone akinesia were randomized to immediate (2 weeks) or delayed (3 months) angioplasty. Repeat catheterization and cardiac magnetic resonance imaging (MRI) were performed after 3 and 12 months. RESULTS: Angiography 3 months after MI revealed that LV ejection fraction (LVEF) had increased ([mean +/- SD] 54.4 +/- 4.3% vs. 63.9 +/- 7.4%, p < 0.01) as a result of improved regional function (p < 0.01) and LV end-systolic volume had decreased (p < 0.002), whereas LV end-diastolic volume remained unchanged. With delayed angioplasty, LVEF, infarct zone wall motion and LV volumes did not improve. Cardiac MRI at baseline and at 3 and 12 months confirmed these findings and extended them up to 1 year, indicating that delayed angioplasty could no longer improve LV function because of marked LV dilation (p < 0.01). Immediate angioplasty had a high success rate, but restenosis (50%) was accompanied by new severe angina as a clinical indicator of salvaged myocardium, which did not occur after delayed angioplasty. CONCLUSIONS: This pilot study in selected patients supports the hypothesis that myocardial viability persists ("hibernation") for 2 to 3 weeks but not for 3 months after MI, during which time it may be worthwhile to restore blood flow to a large myocardial territory, even in asymptomatic patients, to improve long-term LV function.

Electrocardiographic changes during antihypertensive therapy in the International Prospective Primary Prevention Study in Hypertension.

In the International Prospective Primary Prevention Study in Hypertension, electrocardiographic changes before and during 3- to 5-year antihypertensive treatment were investigated in a cohort of 5819 men and women aged 40 to 64 years with entry diastolic blood pressures of 100 to 125 mm Hg. They were randomly allocated to treatment regimens that either included or excluded the slow-release beta-blocker oxprenolol. Electrocardiograms (ECGs) were assessed using the Minnesota Code and assigned to groups of normal ECGs or ECGs with pressure-related, ischemic, "intermediate," or "other" abnormalities. Antihypertensive treatment was associated with a decrease (mainly in men) of pressure-related and (mainly in women) of intermediate abnormalities. Ischemic abnormalities increased, particularly in men. Inclusion of the beta-blocker resulted in a greater reduction in intermediate abnormalities and in a lesser increase in ischemic abnormalities. Better blood pressure control was associated with a lesser increase in ischemic abnormalities and in a regression of pressure-related abnormalities. The presence of ST segment depression and of a complete left bundle branch block in the entry ECG was associated with a significant risk for sudden death and myocardial infarction. Optimal blood pressure control prevents pressure-induced cardiac target organ damage and, hence, heart failure, and may delay the progression of ischemic abnormalities. This tallies with the lower critical cardiac event rate associated with lower blood pressure that was observed in the same study.

Circulatory abnormalities and compensatory mechanisms in heart failure.

Knowledge of the basic alterations of central hemodynamics in congestive heart failure has failed to explain many aspects of this important syndrome. Increasing attention has recently been paid to compensatory and adaptive mechanisms occurring after the initial insult. Thus, new insights have been gained into the pathophysiology of contraction of hypertrophied myocardium and changes of adrenergic receptors in the myocardium due to chronically increased cardiac sympathetic tone. The role of the renin-angiotensin-aldosterone system in early and advanced congestive heart failure has been further elucidated, and the role of the vasodilating atrial natriuretic peptide is undergoing further definition. New results further clarify the mechanisms leading to breathlessness and muscular fatigue in congestive heart failure, with emphasis shifting from the traditional concept of the importance of increased filling pressures to changes to the peripheral circulation and exercising muscles. Although progress has been made in understanding of the pathophysiology of congestive heart failure, many aspects are still poorly understood and await clarification.

Effects of vasodilators on the coronary circulation in congestive heart failure.

Pressure or volume overload of the myocardium increases the wall stress, particularly of the subendocardium, and leads to hypertrophy. Even though cardiac hypertrophy is viewed as a beneficial compensatory process that normalizes wall stress, the increased muscle mass carries with it the need of increased blood supply. Overall flow per unit mass is similar at rest in hypertrophic and normal hearts but a reduction of flow to the subendocardium and an increase in minimal coronary vascular resistance have been described. Thus, the potential exists for a vasodilator-induced steal mechanism shunting blood away from potentially ischemic areas. Angiotensin-converting enzyme inhibitors reduced myocardial oxygen consumption and coronary blood flow in parallel manner in some studies, indicating preserved coronary autoregulation, but there is also some evidence of a coronary vasodilator effect. Calcium antagonists reduce coronary vascular resistance and improve the myocardial demand-supply ratio, but the clinical usefulness of the newer compounds with supposedly little or no negative inotropic effects remains to be established. Hydralazine improved the myocardial oxygen demand-supply ratio in patients with dilated cardiomyopathy, but metabolic function may deteriorate more often after hydralazine than after angiotensin-converting enzyme inhibitors in patients with coronary heart disease. Similar observations have been made using alpha-adrenergic blockers. Although progress has been made in the understanding of the coronary circulation and the influence of vasodilators in congestive heart failure, many questions await clarification using refined or new methodology.

Direct vascular and myocardial effects of nisoldipine.

The effects of the dihydropyridine calcium antagonist nisoldipine on vascular smooth muscle and myocardium were investigated by brachial artery infusions and measurements of forearm blood flow and by intracoronary infusions and measurements of maximal rate of rise of left ventricular pressure (dP/dtmax). Brachial artery infusions (0.1 to 16 micrograms/min/1,000 ml tissue) in 10 patients with essential hypertension increased forearm blood flow and decreased calculated forearm vascular resistance dose dependently (maximal reduction of forearm vascular resistance 88%). A comparison with the vascular effects of verapamil indicated that the vasodilator potency of nisoldipine is approximately 40- to 50-fold greater in this model supporting similar results from in vitro experiments. Coronary artery infusions of nisoldipine (12, 24 and 48 micrograms over 3 minutes each) in 9 patients undergoing diagnostic left-sided cardiac catheterization did not change dP/dtmax. This lack of effect on left ventricular contractility was similar in patients with normal or impaired left ventricular function. Even though the coronary artery concentrations during the infusion are unknown, the highest intracoronary dose was comparable to the highest brachial artery infusion. Since the coronary vasculature has been found to be at least as sensitive to nisoldipine as the peripheral vasculature, it can be assumed that nisoldipine has no negative inotropic effect even in dosages that probably induced marked vasodilation. Thus, for nisoldipine and possibly other new dihydropyridine calcium antagonists, the concept of a dissociation between peripheral vasodilatation and direct myocardial effects also seems to apply to human circulation and the heart.

Combined acebutolol/nifedipine therapy in patients with chronic coronary artery disease: additional improvement of ischemia-induced left ventricular dysfunction.

To assess acute hemodynamic effects of combined oral nifedipine (10 mg) and acebutolol (100 mg), 21 patients with angiographically documented coronary artery disease and stable angina pectoris were studied (three groups of seven randomized patients). Simultaneous hemodynamic and equilibrium radionuclide ejection fraction measurements were performed at rest and during exercise before treatment, 1 hour after administration of nifedipine, acebutolol or a combination of the two and again 1 hour after combined nifedipine and acebutolol. At the same exercise level achieved without drugs, angina, subjectively scored by the patients, decreased significantly after nifedipine, acebutolol and a combination of the two in association with a significant improvement in left ventricular ejection fraction (p less than 0.01). There was an additive effect of both drugs on heart rate, systolic blood pressure and therefore the double product (p less than 0.01 each). The negative effects of acute beta receptor blockade on cardiac index, resting ejection fraction and total peripheral resistance were balanced by the vasodilatory action of nifedipine. In patients with borderline heart failure no untoward effects were seen after combined therapy. Thus, acute combined acebutolol/nifedipine therapy in patients with stable angina proved to be hemodynamically superior to therapy with either drug alone and safe even in patients with moderately depressed left ventricular function. This finding provides a basis for appropriately designed long-term studies.

Beneficial effect of amiodarone on cardiac mortality in patients with asymptomatic complex ventricular arrhythmias after acute myocardial infarction and preserved but not impaired left ventricular function.

To determine whether the beneficial effect of low-dose amiodarone on survival in patients with complex ventricular arrhythmias after myocardial infarction was dependent on left ventricular (LV) function, results of the Basel Antiarrhythmic Study of Infarct Survival were analyzed. Two hundred twelve patients after acute myocardial infarction with asymptomatic complex arrhythmias were randomly assigned to receive amiodarone 200 mg/day or to a control group and followed up for 1 year. Results of mortality and arrhythmic events were related to baseline radionuclide LV ejection fraction. With preserved (greater than or equal to 40%) LV ejection fraction, there was a significantly lower 1-year cardiac mortality in patients treated with amiodarone (1 of 68 or 1.5%) versus control subjects (5 of 56 or 8.9%; p less than 0.03). This was not the case for patients with LV ejection fraction less than 40%. Similarly, arrhythmic events were significantly reduced only in patients with preserved LV function. These results suggest an interaction between the effects of amiodarone on survival and LV dysfunction in patients after acute myocardial infarction. Because of 2 other small studies with similar results, this finding may be of clinical relevance and should be addressed in ongoing and future research with this drug.

Arterial vasodilator, systemic and coronary hemodynamic effects of nisoldipine in congestive heart failure secondary to ischemic or dilated cardiomyopathy.

The systemic and coronary hemodynamic and neurohumoral effects of nisoldipine, a calcium antagonist drug with high vascular specificity, were investigated in 17 patients with chronic congestive heart failure (CHF). Brachial artery infusions (n = 9) decreased forearm vascular resistance in a dose-dependent manner, attesting to its powerful arterial vasodilator properties. A dose of 3 micrograms/kg intravenously decreased mean blood pressure 16% and systemic vascular resistance 33%, while increasing stroke index 19% and ejection fraction 21% at rest and similarly during exercise. Pulmonary capillary wedge pressure decreased significantly during exercise. Intravenous infusion of nisoldipine increased rest coronary sinus flow 10% (p less than 0.05, n = 7), decreased rest and exercise coronary vascular resistance 28% and 19% (p less than 0.01) and rest myocardial oxygen consumption 14% (p less than 0.05). In 13 patients similar systemic hemodynamic results were found after treatment with oral nisoldipine, 2 X 20 mg for 4 weeks. Stroke index and stroke work index increased long-term more than acutely (31% and 12.4% vs 19% and 4.5% at rest, both p less than 0.05), which may indicate a compensated mild cardiodepressant effect of intravenous nisoldipine. Changes in forearm vascular resistance after intra-arterial administration did not correlate with changes of systemic vascular resistance after intravenous administration, suggesting that factors other than vascular calcium entry blockade importantly influence hemodynamic responses. Elevated control plasmas norepinephrine and renin levels, on average, did not change during chronic therapy but individual changes were compatible with a reduction of sympathetic activity in patients with hemodynamic improvement.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive beta blocking action as related to renin and age: a pharmacologic tool to identify pathogenetic mechanisms in essential hypertension.

Three hundred fifteen patients with essential hypertension were classified according to low (18 percent), normal (59 percent) or high (23 percent) renin-sodium index. The proportion of patients with low renin hypertension progressively increased with increasing age and blood pressure, there being no difference between the sexes. Two high renin groups emerged: a younger group with early moderate hypertension, and an older group with severe hypertension consequent to possibly ischemic renal disease. Long-term beta blocking monotherapy in 137 patients resulted in a reduction of idastolic pressure to 95 mm Hg or less in 65 percent: 85 percent in those with high and 73 percent in those with normal renin activity; pressure was reduced to this level in only 1 of 24 patients (4 percent) with a low renin index. Antihypertensive efficacy was also related to age, since diastolic pressure was normalized in 80 percent of patients under age 40 years, in 50 percent of those aged 40 to 60 years, but in only 20 percent of those over age 60 years. Age may heolp in patient selection but is no substitute for the more reliable renin index, especially in patients over age 40 years, or with high pressure. Using studiew with propranolol as a standard, similar renin responses were obtained with two cardioselective beta1 type blocking drugs, atenolol and metoprolol, as well as with two nonselective beta2+1 receptor antagonists, LL21945 exhibiting prolonged receptor affinity and oxprenolol in slow release form. These long-acting drugs, which proved effective in single daily doses, could be of value in improving patient compliance...

Secondary and tertiary prevention with calcium antagonists in coronary artery disease.

Recent multicentre studies evaluating the therapeutic value of calcium antagonists in reducing the incidence of cardiovascular complications after myocardial infarction (secondary prevention) and in retarding the development of atherosclerosis in coronary artery disease (tertiary protection) are reviewed. The prognosis of patients after acute myocardial infarction can be improved not only by interventional measures such as aortocoronary bypass surgery or percutaneous transluminal catheter angioplasty, but also by various drugs. Numerous studies have shown that beta-blockers and platelet aggregation inhibitors can reduce mortality and reinfarction rates. Calcium antagonists in secondary prevention trials after acute myocardial infarction, however, have produced variable results. Whereas the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) [Israeli SPRINT Study Group 1988] with nifedipine showed no beneficial effect of the drug, studies with verapamil in the Danish Verapamil Infarction Trial II (DAVIT II) [Danish Study Group on Verapamil in Myocardial Infarction 1990] and diltiazem in the Multicentre Diltiazem Postinfarction Trial (MDPIT) [Multicenter Diltiazem Postinfarction Trial Research Group 1988] as secondary prevention have demonstrated improvements in survival and cardiovascular complications, but these improvements were restricted to patients without heart failure. In view of the ability of calcium antagonists to reduce atheroma progression in coronary artery disease in animal models, the antiatherosclerotic effects of these agents in clinical studies have generally been disappointing. In the International Nifedipine Trial on Antiatherosclerotic Therapy (INTACT) [Lichtlen et al. 1990], however, nifedipine treatment was associated with a 28% reduction in new lesion development, but did not affect the development of severe lesions. Similar results have been obtained with nicardipine.

Effect of short and long term administration of amiodarone on ischaemia-induced left ventricular dysfunction. Implications for combined antianginal drug therapy.

To asses haemodynamic effects of short and long term amiodarone on ischaemia-induced left ventricular dysfunction and to compare them with those of glyceryl trinitrate (nitroglycerin), beta-blocking and calcium antagonist drugs, 19 patients with chronic ischaemic heart disease were studied. All patients underwent simultaneous right heart catheterisation and equilibrium radionuclide angiocardiography at rest and during symptom-limited supine bicycle exercise. After control measurements without antianginal therapy, 10 patients received 7.5 mg/kg amiodarone intravenously over 5 minutes (short term study) followed by oral administration of amiodarone for 3 weeks (long term study). The remaining 9 patients were studied following the randomised administration of glyceryl trinitrate (0.8 mg sublingually), metoprolol (0.15 mg/kg intravenously) and nifedipine (5 ng/kg/min). During exercise known to provoke angina pectoris without therapy (control study), amiodarone improved myocardial oxygen consumption by reducing heart rate and systolic blood pressure without the negative inotropic effects seen after acute beta-adrenoceptor blockade. Comparisons with the haemodynamic profiles of other antianginal drugs suggest that amiodarone may be most effective when combined with glyceryl trinitrate or nifedipine for the treatment of ischaemic left ventricular dysfunction.

Cilazapril in congestive heart failure. A pilot study.

The haemodynamic effects of a single dose of cilazapril 2.5 or 5 mg were studied in 33 patients with stable chronic congestive heart failure who were receiving digitalis and diuretics. Subsequently, a double-blind comparison of the haemodynamic and clinical effects of 3 months' treatment with cilazapril 1.25 to 5 mg daily or placebo in 24 evaluable patients revealed that the acute haemodynamic improvement produced by a single dose of cilazapril was maintained in patients receiving repeated administration of the drug, but not in those randomly allocated the placebo. Acute cilazapril significantly decreased mean arterial pressure, systemic vascular resistance, pulmonary capillary wedge pressure, pulmonary artery pressure and right atrial pressure, while cardiac index and stroke volume index increased at rest and during submaximal exercise. After 3 months' treatment 11 of 13 cilazapril recipients improved their New York Heart Association (NYHA) class compared with 2 of 11 patients treated with placebo. This functional improvement was paralleled by a patient-perceived improvement in general well-being.

Coronary artery bypass grafts. Influence of preoperative risk factors on the late postoperative course.

In order to assess the influence of preoperative risk factors on the late postoperative course, 186 consecutive patients in whom coronary artery bypass graft (CABG) was performed for chronic stable angina (169 men, 17 women, mean age +/- SD 54 +/- 8 years) were followed for an average of 54 (6 to 113) months. The overall five-year survival rate by life-table analysis was 90 +/- 2 percent. The postoperative course was considered favorable in 112 patients (60 percent) in whom angina was absent or improved by at least 2 NYHA classes throughout the entire follow-up, and was unsatisfactory in 74 patients. It was concluded that the late postoperative course of patients with CABG was unfavorably influenced by the presence of two or three risk factors, and a high preoperative cholesterol level was the only single risk factor associated with unsatisfactory outcome.

Clinical risk assessment after first myocardial infarction--is additional noninvasive testing necessary?

In order to assess whether the outcome of MI can be predicted by clinical data alone or whether and how much noninvasive testing is necessary to predict cardiac events or death, 361 patients were prospectively evaluated and followed for up to five years. A recursive partitioning analysis indicated that high-risk patients can be identified clinically after MI with a high degree of accuracy; to separate low-risk patients who need no further investigation or therapy, however, one additional noninvasive test is necessary which allows quantification of myocardial damage as well as exercise-induced ischemia. Additional tests added little to this risk prediction, indicating that multiple noninvasive testing should not be performed.

Plasma adrenaline and noradrenaline in patients with acute myocardial infarction. Relationship to ventricular arrhythmias of varying severity.

Plasma adrenaline (A) and noradrenaline concentrations (NA) were determined in 41 patients admitted to the coronary care unit (CCU). Eleven with suspected acute myocardial infarction (AMI), subsequently excluded as a diagnosis, had significantly elevated A and NA compared with 20 normal resting subjects. Patients with proven infarcts but no ventricular fibrillation had even higher levels of A and NA. Nine patients with ventricular fibrillation as a complication of AMI showed the highest plasma catecholamine values on admission. Patients with AMI and congestive heart failure exhibited substantially increased A, while NA was only slightly elevated compared with that of AMI patients without congestive heart failure. High plasma catecholamines and the relationship between adrenaline and the severity of ventricular arrhythmias suggest that the sympathetic nervous system plays an important role in sustaining a vicious circle of increased myocardial damage and increased irritability during the acute phase of AMI.

Persisting symptoms despite permanent pacing. Incidence, causes, and follow-up.

Persisting symptoms, consisting of palpitations, dizziness, or syncope, were found in 49 of 570 consecutively followed patients (8.6 percent) with permanent pacemakers (PM). Among 540 patients with ventricular PM, 19 had syncope and 24 dizziness; among 30 patients with dual-chamber PM, five had palpitations and one dizziness. Symptoms were PM-related in 17, caused by tachyarrhythmias in 12, of noncardiac origin in 16, and of unknown origin in four patients. Holter monitoring was necessary for evaluating the persisting symptoms in 36 patients and helpful in 32 studies (89 percent). Symptoms were relieved in all patients with PM-related causes but only in 6/16 patients (38 percent) with syncope or dizziness of noncardiac origin despite various therapeutic measures. In patients with either documented tachyarrhythmias or unknown cause of syncope or dizziness, antiarrhythmic drugs led to symptomatic improvement in 11 of 12 treated patients during an average follow-up of 15 months. We concluded that: (1) persistent syncope, dizziness, or palpitations occurred in 8.6 percent of 570 patients after PM-implantation; (2) symptoms were more frequent but less severe in patients with dual-chamber PM than in those with ventricular PM; (3) tachyarrhythmias as a possible cause of symptoms were found in 25 percent of patients; (4) symptomatic improvement was noted in 28 of 29 patients when a PM-related cause or tachyarrhythmias were treated.