Utility of introducing ventricular premature complexes during reciprocating tachycardia in specifying the location of left free wall accessory pathways.

The usefulness of the response to single and double ventricular premature complexes (VPCs) introduced during reciprocating tachycardia (RT) in predicting the location of a left free wall accessory pathway was studied in 55 patients with the Wolff-Parkinson-White syndrome. One VPC introduced from the right ventricle into narrow QRS RT when the His bundle was refractory resulted in retrograde atrial preexcitation in 25 of 55 (45%) patients, while 30 (55%) showed no preexcitation. Double VPCs produced retrograde atrial preexcitation in 9 of 26 patients not responding to a single VPC. No difference in RT cycle length, AH, HV or ventriculoatrial intervals was found between those patients who did or did not show retrograde atrial preexcitation. The response to single and double VPCs during RT was related to the location of the AP. The average distance of the AP from the crux determined by intraoperative epicardial mapping in the 41 patients who underwent surgery was 2.7 +/- 0.7 mapping units (left posterolateral region) in patients showing retrograde atrial preexcitation with a single VPC, 3.6 +/- 0.7 units (at the lateral left ventricular margin) in those responding to double VPCs and 4.3 +/- 0.8 units (beyond the LV margin) in those showing no response. Left bundle--branch block (LBBB) aberrancy during RT resulted in an average 60 +/- 14 ms prolongation of the ventriculoatrial interval in 40 patients, including 5 in whom LBBB was seen only after procainamide infusion. VPCs introduced into LBBB RT resulted in significant retrograde atrial preexcitation in 6 additional patients in whom no response during normal QRS RT was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Late restenosis after emergent coronary angioplasty for acute myocardial infarction: comparison with elective coronary angioplasty.

The late restenosis rate after emergent percutaneous transluminal coronary angioplasty for acute myocardial infarction was assessed by performing outpatient follow-up cardiac catheterization in 79 (87%) of 91 consecutive patients who had been discharged from the hospital with a successful coronary angioplasty. The majority of patients (90%) received high dose intravenous thrombolytic therapy with streptokinase in addition to angioplasty. Similar follow-up data were obtained in 206 (90%) of 228 consecutive patients who had successful elective angioplasty during the same period. The interval from angioplasty to follow-up was 28 +/- 9 weeks for the myocardial infarction group and 30 +/- 11 weeks for the elective group. Baseline clinical variables were similar for both the myocardial infarction and elective groups except for a higher percentage of men in the infarction group (81 versus 63%, p = 0.001). The number of coronary lesions undergoing angioplasty and the incidence of intimal dissection were similar, but multivessel angioplasty was more common in the elective group (13 versus 4%, p = 0.02). The rate of in-hospital reocclusion was higher in the patients receiving angioplasty for myocardial infarction (13 versus 2%, p = 0.0001). At the time of late follow-up after hospital discharge, the patients with myocardial infarction were more often asymptomatic (79 versus 55%, p = 0.0001), and the rate of angiographic coronary restenosis was lower for the infarction group both overall (19 versus 35%, p = 0.006) and when multivessel angioplasty patients were excluded (19 versus 33%, p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary perfusion during acute myocardial infarction with a combined therapy of coronary angioplasty and high-dose intravenous streptokinase.

Two hundred and sixteen patients with acute myocardial infarction were treated with immediate infusion of high-dose (1.5 million units) intravenous streptokinase followed by emergency coronary angioplasty. The infarct lesion was crossed and dilated in 99% and persistent coronary perfusion after the procedure was achieved in 90% (including 3% with significant residual stenosis). Total in-hospital mortality was 12%. Multivariable analysis showed a higher hospital mortality with cardiogenic shock (41% vs 5% without shock), older age, lower left ventricular ejection fraction, and female sex. Final patency of the infarct-related vessel was determined by follow-up in-hospital cardiac catheterization. Coronary reocclusion occurred in 11% (symptomatic in 7%, treated with emergency angioplasty or bypass surgery; silent in 4%, treated medically). Of the surviving patients with successful initial establishment of infarct vessel patency, 94% were discharged from the hospital with an open infarct artery or a bypass graft to the infarct vessel. There was significant improvement in both ejection fraction (44% to 49%; p less than .0001) and regional wall motion in the infarct zone (-3.0 SD to -2.4 SD; p less than .0001) among patients with persistent coronary perfusion and insignificant residual stenosis at the time of the follow-up cardiac catheterization. Thus, a treatment strategy for acute myocardial infarction that includes immediate administration of streptokinase followed by emergency coronary angioplasty, and coronary bypass surgery when necessary, results in a high rate of early and sustained patency of the infarct-related vessel.

Medical approaches to prevention of restenosis after coronary angioplasty.

Although initial success rates for coronary angioplasty have improved, the rate of restenosis within 6 months of the procedure has persisted at 30 to 40%. The relation of restenosis to initial success, recurrence of symptoms and risk factors suggests that high grade or total lesions, long lesions, lesions in the proximal left anterior descending artery or in saphenous grafts, and the absence of intimal dissection after angioplasty are associated with an increased risk of restenosis. Unstable angina, male sex and diabetes are clinical factors associated with a greater risk of restenosis. Pathologic specimens suggest that plaque splitting and disruption are found acutely after angioplasty, but that restenosis occurs as an excessive reparative, proliferative response of smooth muscle cells leading to recurrent luminal narrowing. A prospective analysis of therapeutic interventions to prevent restenosis, such as administering antiplatelet and lipid-lowering agents, intensive diabetic therapy and administration of calcium antagonists, is proposed. Problems with timing of studies, design and sample size are considered. Current recommendations for anti-restenosis therapy include antiplatelet therapy before and after angioplasty, administration of heparin in some patients and intensive risk factor intervention for the 6 months after the procedure.

Frequency, diagnosis and clinical characteristics of patients with multiple accessory atrioventricular pathways.

Multiple accessory atrioventricular (AV) pathways were documented in 52 of 388 patients (13%) who underwent detailed electrophysiologic evaluation. Multiple AV pathways were identified during intraoperative mapping or electrophysiologic study by different patterns of ventricular preexcitation during atrial fibrillation, flutter or atrial pacing with different delta-wave morphologic and ventricular activation patterns; different sites of atrial activation during right ventricular pacing or orthodromic reciprocating tachycardia; or preexcited reciprocating tachycardia using a second pathway as the retrograde limb of the tachycardia. A logistic model was used to determine which clinical, electrocardiographic and electrophysiologic variables were associated with multiple AV pathways. Right free-wall and posteroseptal accessory AV pathways were more common in patients with multiple AV pathways and were frequently associated. Multivariate logistic regression identified Ebstein's anomaly, and a history of preexcited reciprocating tachycardia as significant variables (p less than 0.0001). Pathway location was not subjected to statistical analysis because of confounding variables.

Characterization of retrograde conduction by direct endocardial recording from an accessory atrioventricular pathway.

Accessory pathway electrograms are rarely recorded in patients with Wolff-Parkinson-White syndrome. In one patient, during electrophysiologic study, simultaneous local ventricular (V) accessory pathway (AP) and atrial (A) deflections were recorded during bipolar catheter endocardial mapping over the pathway. Analysis of changes in electrographic intervals during performance of the ventricular extrastimulus technique allowed characterization of the retrograde conduction properties of the pathway. As coupling intervals were decreased, an initial increase was seen in the AP2A2 interval with subsequent ventriculoatrial block between the accessory pathway and atrium. When coupling intervals were further decreased, the V2AP2 interval lengthened with ultimate block between the ventricle and accessory pathway. These findings support the concept of impedance mismatch as the cause of conduction block in accessory pathways with the distal junction of the accessory pathway being the most vulnerable.

Cardiac function in patients on chronic amiodarone therapy.

Antiarrhythmic agents may depress cardiac contractility and worsen heart failure. Few data are available describing the chronic effects of amiodarone on myocardial function. To assess the effects of amiodarone on cardiac function, we studied 41 consecutive patients with first-pass or equilibrium radionuclide angiography prior to and 3 months after drug therapy was initiated. The mean heart rate, systolic blood pressure (BP), and diastolic BP were not significantly altered by treatment. The mean ejection fraction was 36% +/- 19 (mean +/- 1 SD) at the time of drug initiation and 36% +/- 17 3 months later (p less than 0.05). Nineteen patients had an ejection fraction greater than 30% and 16 had an ejection fraction less than 30%. The mean change in ejection fraction for these two subgroups showed no statistically significant difference, although a decrease in EF greater than 10% was seen in three patients (symptomatic in two), necessitating an increase in diuretic dose. No correlation between amiodarone dose and change in ejection fraction (r = -0.12, p greater than 0.05) was noted. There was no correlation between baseline ejection fraction and change in ejection fraction over this 3-month period (r = -0.36, p greater than 0.05). In summary, amiodarone does not depress left ventricular function and as a result can be used safely in patients with mild to moderate impairment of left ventricular function. In patients with stable left ventricular function, serial tests of left ventricular function may not be necessary.

Frequency-dependent effects of verapamil on atrioventricular nodal conduction in man.

We sought to determine if verapamil induces frequency-dependent prolongation of atrioventricular nodal conduction in 10 consecutive patients studied in the electrophysiology laboratory. We used a maintenance infusion of verapamil designed to produce plasma concentrations of verapamil in the "therapeutic" range and that did not alter heart rate or blood pressure significantly. Frequency-dependent prolongation of atrioventricular nodal conduction (AH interval) was demonstrated in all 10 patients (p less than .001), and no change in HV conduction time with decreasing cycle length was noted in any patients while receiving verapamil. Two patterns of use-dependent response were seen. In four patients frequency-dependent prolongation of the delta(AH) interval [delta(AH) = AHverapamil - AHcontrol at a given cycle length] was seen with each decrement in pacing cycle length. In six patients frequency-dependent prolongation of the delta(AH) interval was not manifest until the fifth to eighth pacing cycle length tested. There was no association between the pattern observed and the initial heart rate or AH interval. After an abrupt change in pacing cycle length, the kinetics of delta (AH) interval prolongation were rapid; equilibrium was achieved by five to eight pulses in all patients. There was no correlation between the magnitude of prolongation of the AH interval noted at a particular cycle length and the concentration of verapamil during the maintenance infusion. These results indicate that verapamil causes use-dependent prolongation of atrioventricular nodal conduction in man.

Comparative response of male and female patients with coronary artery disease to exercise rehabilitation.

Male (227) and female (37) participants in a supervised rehabilitation programme for patients with coronary artery disease were compared in relation to their compliance with and response to the programme. The drop-out rate was higher in females (18.9% vs 7.9%) and their attendance rate at sessions was lower (77% vs 87%). Following the programme, exercise duration was significantly increased in both groups to a similar degree, although absolute values were consistently higher in males. The heart rates required to perform given workloads were reduced for both sexes, the magnitude of reduction being similar. Blood pressure was not altered after rehabilitation. These findings show that female patients, despite poorer compliance than males, can benefit equally from exercise rehabilitation.

Antihypertensive and renal haemodynamic effects of atenolol and nadolol in elderly hypertensive patients.

As little is known of the antihypertensive efficacy or renal haemodynamic effects of beta-adrenoceptor blocking drugs in the elderly we studied two such drugs, atenolol and nadolol, in elderly hypertensive patients. Ten patients took part in a placebo-controlled double-blind study of atenolol and 10 received nadolol in a single-blind placebo-controlled study. Treatment phases lasted 12 weeks for atenolol or 10 weeks for nadolol. Blood pressure, effective renal blood flow and glomerular filtration rate data obtained at the end of each treatment phase were analysed. Atenolol lowered mean arterial pressure (mean +/- s.e. mean) from 129.9 +/- 1.5 to 108.2 +/- 2.3 mm Hg (P less than 0.01) while it increased mean effective renal blood flow 512.5 +/- 86.6 to 646.0 +/- 116.1 ml min-1 1.73 m-2 (P less than 0.05). Nadolol reduced mean arterial pressure from 133.2 +/- 2.0 to 113.5 +/- 3 mm Hg (P less than 0.001) but reduced mean effective renal blood flow from 558.8 +/- 32.2 to 446.0 +/- 26.9 ml min-1 1.73 m-2 (P less than 0.05). Glomerular filtration did not alter significantly with either drug. We conclude that beta-adrenoceptor blocking drugs are effective antihypertensive agents in the elderly but have disparate effects on effective renal blood flow perhaps because of differences in cardioselectivity. These data suggest that comparative studies with thiazide diuretics and beta-adrenoceptor blocking drugs are warranted in elderly hypertensives.

Clinical and haemodynamic responses to captopril and hydralazine in chronic congestive heart failure: the importance of preload reduction.

1 Although many vasodilators are effective in the treatment of severe congestive heart failure, there have been few comparative studies of these drugs. We compared the acute haemodynamic effects of captopril and hydralazine in 11 patients with congestive cardiac failure unresponsive to diuretics and digoxin. Both drugs increased resting cardiac index, although this effect appeared more pronounced for hydralazine (33% v 23%). Captopril reduced pulmonary capillary wedge pressure (-8 mm Hg, p less than 0.01) which decreased only slightly on hydralazine. 2 Long-term treatment was then started on the dose found effective during acute administration. Each drug was given for eight weeks. Exercise tolerance improved with both drugs, the increase during the hydralazine phase correlating with the increase in cardiac index at rest (r = 0.75; p less than 0.05). Clinical improvement appeared more definite on captopril than on hydralazine, however. This improvement was maintained during the captopril phase only in those patients who had a greater than 25% reduction in pulmonary capillary wedge pressure in the acute study.

Accuracy of the London School of Hygiene and Remler M2000 sphygmomanometers.

1. The accuracy of the Remler M2000, a semiautomatic portable blood pressure recorder, was assessed with the London School of Hygiene (LSH) and Hawkesley random-zero sphygmomanometers used as reference standards. 2. The Remler gave higher recordings than the LSH sphygmomanometer, the mean systolic and diastolic differences being 5.9 mmHg (P less than 0.001) and 4.7 mmHg (P less than 0.001) respectively. No significant difference was demonstrated between paired Remler and Hawkesley recordings. 3. When simultaneous paired LSH and Hawkesley sphygmomanometer recordings were compared, with LSH gave lower blood pressures: 7.1 mmHg (P less than 0.001) for systolic and 3.6 mmHg (P less than 0.001) for diastolic recordings. 4. The LSH sphygmomanometer underestimates blood pressure, partly due to a calibration error but also because the selection of end points for this device differs from other methods of blood pressure measurement.