Effects of percutaneous transluminal coronary angioplasty on exercise-induced changes in R-wave amplitude.
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
D R Rosing
Publications and source records attributed to D R Rosing.
Surgical removal of the intracoronary portion of a fractured angioplasty guidewire.
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Angioplasty, Balloon↗
Relation between serum nifedipine concentration and hemodynamic effects in nonobstructive hypertrophic cardiomyopathy.
The relation between nifedipine concentration and hemodynamic effects after sublingual administration of 10 or 20 mg was examined in 13 patients with nonobstructive hypertrophic cardiomyopathy (HC). Serum nifedipine concentrations were determined by gas chromatography and were not related to dose. Peripheral vascular resistance decreased as a function of nifedipine concentration (r = -0.63, p less than 0.001); this was associated with a concentration-related increase in heart rate (r = 0.56, p less than 0.001) and in cardiac index (r = 0.50, p less than 0.001). However, evidence for a pure vasodilator effect of nifedipine was inconsistent, in that the change in stroke volume index with nifedipine was not significant. Although stroke volume index increased at nifedipine concentrations between 60 and 120 ng/ml (38 +/- 6 to 42 +/- 4 ml/m2, p less than 0.01), it decreased at concentrations greater than 120 ng/ml (40 +/- 3 to 38 +/- 4 ml/m2, p less than 0.01). Moreover, pulmonary artery wedge pressure increased at nifedipine concentrations greater than 120 ng/ml (11 +/- 2 to 16 +/- 4 mm Hg, p less than 0.001), suggesting either depressed left ventricular (LV) systolic function or reduced LV filling. To investigate these possible mechanisms, LV systolic and diastolic function was studied during catheterization with a nonimaging scintillation probe in 6 of the 13 patients. In these subjects, heart rate was held constant by atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[The diastolic function in hypertrophic cardiomyopathy].
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Cardiomyopathy, Hypertrophic↗
Three year anatomic, functional and clinical follow-up after successful percutaneous transluminal coronary angioplasty.
Because the long-term anatomic effects of percutaneous transluminal coronary angioplasty are unknown, follow-up evaluations including coronary angiography, treadmill exercise testing and rest and bicycle exercise radionuclide angiography were performed in 46 patients 6.3 +/- 2.0 and 37.6 +/- 3.6 (mean +/- SD) months after they had undergone successful single lesion angioplasty. The severity of the coronary stenosis decreased significantly at each evaluation; the mean diameter stenosis was 66 +/- 13% before angioplasty, 30 +/- 13% immediately after and 26 +/- 16% and 19 +/- 13% at 6 months and 3 years, respectively. Exercise time increased from 9.8 +/- 4.4 minutes before angioplasty to 18.3 +/- 4.5 minutes immediately after the procedure and remained at that level at 6 months (20.3 +/- 4.6 minutes) and 3 years (18.2 +/- 4.5 minutes). Left ventricular ejection fraction during exercise decreased 4 +/- 6% compared with rest before angioplasty, but increased 7 +/- 7% immediately after angioplasty and this increase was maintained at 6 months (+/- 6 +/- 7%) and 3 years (+/- 4 +/- 6%). Before angioplasty, 1 patient was in Canadian Heart Association functional class 0, 15 were in class II, 24 in class III and 6 in class IV. Three years later, 25 were in class 0, 10 in class I, 7 in class II and 4 in class III. These results indicate that the short-term anatomic and functional success of coronary angioplasty is maintained for at least 3 years.
Adult↗
Differences in coronary flow and myocardial metabolism at rest and during pacing between patients with obstructive and patients with nonobstructive hypertrophic cardiomyopathy.
Fifty patients with hypertrophic cardiomyopathy underwent invasive study of coronary and myocardial hemodynamics in the basal state and during the stress of pacing. The 23 patients with basal obstruction (average left ventricular outflow gradient, 77 +/- 33 mm Hg; left ventricular systolic pressure, 196 +/- 33 mm Hg, mean +/- 1 SD) had significantly lower coronary resistance (0.85 +/- 0.18 versus 1.32 +/- 0.44 mm Hg X min/ml, p less than 0.001) and higher basal coronary flow (106 +/- 20 versus 80 +/- 25 ml/min, p less than 0.001) in the anterior left ventricle, associated with higher regional myocardial oxygen consumption (12.4 +/- 3.6 versus 8.9 +/- 3.3 ml oxygen/min, p less than 0.001) compared with the 27 patients without obstruction (mean left ventricular systolic pressure 134 +/- 18 mm Hg, p less than 0.001). Myocardial oxygen consumption and coronary blood flow were also significantly higher at paced heart rates of 100 and 130 beats/min (the anginal threshold for 41 of the 50 patients) in patients with obstruction compared with those without. In patients with obstruction, transmural coronary flow reserve was exhausted at a heart rate of 130 beats/min; higher heart rates resulted in more severe metabolic evidence of ischemia with all patients experiencing chest pain, associated with an actual increase in coronary resistance. Patients without obstruction also demonstrated evidence of ischemia at heart rates of 130 and 150 beats/min, with 25 of 27 patients experiencing chest pain. In this group, myocardial ischemia occurred at significantly lower coronary flow, higher coronary resistance and lower myocardial oxygen consumption, suggesting more severely impaired flow delivery in this group compared with those with obstruction. Abnormalities in myocardial oxygen extraction and marked elevation in filling pressures during stress were noted in both groups. Thus, obstruction to left ventricular outflow is associated with high left ventricular systolic pressure and oxygen consumption and therefore has important pathogenetic importance to the precipitation of ischemia in patients with hypertrophic cardiomyopathy. Patients without obstruction may have greater impairment in coronary flow delivery during stress.
Adult↗
Inducible polymorphic ventricular tachycardia and ventricular fibrillation in a subgroup of patients with hypertrophic cardiomyopathy at high risk for sudden death.
This investigation was undertaken to elucidate the underlying electrophysiologic substrate in hypertrophic cardiomyopathy and to identify possible predictors of sudden death in this patient population. Programmed stimulation was performed in 18 patients aged 14 to 64 years (mean 36) believed to be at high risk for sudden death on the basis of prior cardiac arrest or syncope, nonsustained ventricular tachycardia on Holter ambulatory electrocardiographic (ECG) monitoring or a family history of frequent sudden death. Polymorphic ventricular tachycardia that deteriorated to ventricular fibrillation was reproducibly induced in 8 (44%) of the 18 patients (Group A). This rhythm was induced in all three patients with a history of cardiac arrest. No sustained monomorphic ventricular tachycardia was induced. Group B comprised the 10 patients in whom a sustained arrhythmia could not be reproducibly initiated. The electrophysiologic substrate was distinctly different in patients with, than in those without, inducible sustained arrhythmia. The refractory period was shorter at the right ventricular outflow tract (232 +/- 22 ms) compared with the apex (264 +/- 12 ms) in Group A (p less than 0.005) whereas there was no difference in Group B (271 +/- 25 ms versus 271 +/- 13 ms). The local ventricular electrogram of most patients in both groups was prolonged and markedly multiphasic. However, 5 of the 8 Group A patients exhibited a double electrogram (V-V') with premature stimulation compared with 1 of the 10 patients in Group B (p less than 0.02). A positive R wave in lead aVR of the scalar ECG and poor R wave progression in the precordial leads were more common in Group A than in Group B (p less than 0.001 and p less than 0.001, respectively). The reason for the distinctly different electrophysiologic substrate and the high prevalence of inducible polymorphic arrhythmia is unclear. It may relate to the underlying myocardial architecture in these patients, characterized by myocardial cellular disarray and fibrosis.
Adolescent↗
Limited coronary flow reserve after dipyridamole in patients with ergonovine-induced coronary vasoconstriction.
Patients with anginal chest pain despite angiographically normal coronary arteries and left ventricles may have abnormalities of coronary flow reserve. Twenty-five patients were found to have limited flow reserve during rapid atrial pacing after administration of 0.15 to 0.30 mg iv ergonovine, associated with precipitation of chest pain and hemodynamic and metabolic evidence of myocardial ischemia. No significant narrowing occurred in epicardial coronary artery luminal diameter. An additional 15 patients had no chest pain during pacing; because they developed significantly higher great cardiac vein flow and lower coronary resistance they were considered to have normal vasodilator reserve. After administration of dipyridamole (0.5 to 0.75 mg/kg iv), the lowest absolute levels to which coronary resistance fell (0.79 +/- 0.23 vs 0.47 +/- 0.12 mm Hg X min/ml; p less than .001) and the maximal absolute levels to which great cardiac vein flow rose (134 +/- 34 vs 202 +/- 45 ml/min; p less than .001) were impaired in the 25 patients with ergonovine-induced flow limitation compared with the 15 patients without flow limitation after ergonovine. In addition, 18 of the 25 patients with limited flow reserve after dipyridamole experienced chest pain despite an increase in coronary flow. In these patients, dipyridamole-induced increased flow across small prearteriolar coronary arteries, which were narrowed because of abnormal tonus or sensitivity to vasoconstrictor stimuli, could have resulted in a transmural redistribution of blood flow away from the subendocardium, precipitating subendocardial ischemia. These studies suggest that patients with anginal chest pain despite normal epicardial coronary arteries may have exaggerated coronary responses to vasoconstrictor stimuli, which can result in myocardial ischemia during stress, as well as attenuated responses to coronary vasodilator stimuli.
Adult↗
Impaired left ventricular systolic and diastolic function without left ventricular dilatation associated with papillary muscle calcification in hypertrophic cardiomyopathy.
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Calcinosis↗
Indices of sympathetic vascular innervation in sympathectomized patients.
We measured arterial and venous plasma catecholamines and used laser-Doppler flowmetry to measure cutaneous microcirculatory flow in the sympathectomized and in the intact limbs of 3 patients who had undergone regional sympathectomies. Venous concentrations of norepinephrine, the sympathetic neurotransmitter, exceeded arterial concentrations in the intact limbs--a normal finding--but invariably were less than arterial in the sympathectomized limbs of the same patients, both during baseline conditions and during sympathetic stimulation using tilt, standing and the cold pressor test (mean arteriovenous decrement about 40%). Arterial epinephrine levels exceeded venous levels with or without sympathectomy. Skin microvascular flow rapidly decreased during the cold pressor test and the Valsalva maneuver in the intact but not in the sympathectomized limbs, and spontaneous flow oscillations occurred in the sympathectomized limbs. The results suggest that an arteriovenous increment in plasma norepinephrine reflects local release of norepinephrine from sympathetic nerve endings, whereas removal of circulating catecholamines can occur with or without sympathetic neural impulses. Laser-Doppler flowmetry can measure reflexive sympathetically mediated responses of skin microvascular flow and so can detect sympathetic denervation. Spontaneous oscillations in this flow may not depend exclusively on oscillations in the activity of the sympathetic microvascular innervation.
Adult↗
Isovolumic relaxation period in hypertrophic cardiomyopathy: assessment by radionuclide angiography.
Left ventricular isovolumic relaxation and the relation between relaxation and filling were studied in 90 patients with hypertrophic cardiomyopathy and 29 control subjects using radionuclide angiography. The isovolumic relaxation period was determined automatically on left ventricular time-activity curves as the interval between minimal volume and onset of rapid filling. In 17 patients, M-mode echocardiography performed simultaneously with radionuclide angiography demonstrated that onset of mitral valve opening correlated well with onset of rapid filling (r = 0.84, p less than 0.001). The isovolumic relaxation period was longer in patients with hypertrophic cardiomyopathy than in control subjects (95 +/- 44 versus 50 +/- 23 ms, p less than 0.01) and was longer in patients without an outflow tract gradient at rest than in patients with a gradient (109 +/- 37 versus 86 +/- 35 ms, p less than 0.05). In these patients without obstruction, a weak linear relation between duration of the isovolumic period and peak filling rate was found (r = 0.48, p less than 0.02). Filling was impaired in patients with hypertrophic cardiomyopathy, as assessed by lower peak filling rate (3.2 +/- 1.2 versus 3.5 +/- 0.5 end-diastolic volume/s, p less than 0.05) and prolonged time to peak filling rate (185 +/- 44 versus 145 +/- 20 ms, p less than 0.01) compared with values in control subjects. The delay in time to peak filling rate was caused primarily by the prolonged isovolumic period, because the interval from onset of rapid filling to peak filling rate was similar in patients with hypertrophic cardiomyopathy and control subjects (87 +/- 31 versus 95 +/- 25 ms, NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Left ventricular pulsus alternans in patients with hypertrophic cardiomyopathy and severe obstruction to left ventricular outflow.
Left ventricular pulsus alternans (LVPA), a rhythmic beat to beat variation in left ventricular systolic pressure and outflow gradient, was noted in 35 of 200 ventricular systolic pressure and outflow gradient, was noted in 35 of 200 patients with hypertrophic cardiomyopathy undergoing hemodynamic study. LVPA was not associated with significant systemic pulsus alternans nor right ventricular pulsus alternans. All patients with LVPA had severe outflow gradients at rest or during provocation. Of 61 patients with severe basal outflow gradients (greater than 80 mm Hg), 12 demonstrated LVPA at rest. Eight of these patients underwent ventricular septal myotomy-myectomy; all had successful abolition of basal outflow gradient. Of the seven of these eight patients who underwent postoperative hemodynamic study and who were in sinus rhythm, none demonstrated LVPA. Eleven of 60 patients with basal outflow gradients ranging from 10 to 70 mm Hg demonstrated LVPA during maneuvers provocative for outflow gradients (mean gradient 90 +/- 37 mm Hg). Two of these patients underwent ventricular septal myotomy-myectomy; neither had a gradient nor LVPA during provocation postoperatively. Twelve additional patients with basal outflow gradients ranging from 0 to 115 mm Hg had LVPA after ectopic beats, generally occurring during maneuvers provocative for outflow gradients, associated with severe outflow gradients (mean gradient 130 +/- 39 mm Hg) during the postextrasystolic beat. None of the 41 patients without an outflow gradient, basal or during provocation, was found to have LVPA. Thus LVPA is commonly seen in during provocation, was found to have LVPA. Thus LVPA is commonly seen in patients with hypertrophic cardiomyopathy and severe left ventricular outflow gradients and may represent inadequate left ventricular contractile function in the presence of high left ventricular systolic pressures.
Adult↗
Efficacy of calcium channel blocker therapy for angina pectoris resulting from small-vessel coronary artery disease and abnormal vasodilator reserve.
Abnormal vasodilator reserve of the coronary microcirculation is a frequent mechanism of angina pectoris in patients with angiographically normal coronary arteries. To assess the effect of calcium channel blocking agents on symptoms and exercise capacity, 26 patients shown to have angina pectoris because of abnormally small coronary arteries and limited vasodilator reserve underwent randomized, double-blind, placebo-controlled outpatient study, with 1 month for each period. An unblinded lead-in phase determined the best dose of verapamil (17 patients) or nifedipine (9 patients). Exercise testing using bicycle ergometry was performed at the end of each period. Four patients interrupted the placebo period and 1 patient interrupted both placebo and drug period because of frequent and severe chest pain. While receiving calcium channel blocker drugs, patients who completed both phases of the study recorded fewer episodes of angina (21 +/- 21 vs 35 +/- 27, p less than 0.001) and consumed fewer nitroglycerin tablets (23 +/- 27 vs 41 +/- 50, p less than 0.001) than during the placebo period. Exercise duration was slightly but significantly prolonged (278 +/- 129 vs 231 +/- 136 seconds, p less than 0.025) during drug treatment compared with placebo, and significantly fewer patients terminated exercise with chest pain while receiving drug treatment. Subjectively, 22 of 26 patients felt better on the calcium channel blocker than on placebo. Thus, calcium channel blocker therapy appears to be beneficial in controlling angina and improving exercise tolerance in patients with angina pectoris resulting from abnormally small coronary arteries and limited vasodilator reserve.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Coronary angioplasty: clinical and angiographic follow-up.
To evaluate the clinical status and restenosis rate after percutaneous transluminal coronary angiography (PTCA), 251 consecutive patients who had undergone a successful procedure from February 1979 to May 1983 were studied. Angiography was done routinely in 92 of the initial 100 consecutive patients in whom the procedure was successful (group I), 1 to 11 months (mean 6) after PTCA. Restenosis occurred in 37 of 92 patients (40%); all but 2 (who had collateral flow to the restenosed vessel) had symptoms. Conversely, 44 of 46 asymptomatic patients had no restenosis. The other 159 patients (group II) were followed up clinically, with angiography performed only if signs or symptoms of ischemia recurred. Restenosis suspected clinically and confirmed angiographically occurred in 35 of 92 patients (38%) in group I and 36 of 154 patients (23%) in group II. Of 251 patients with follow-up of at least 6 months, 109 patients (43%) became symptomatic. Of 109 symptomatic patients, 104 consented to coronary angiography; restenosis was found in 67%, progression of narrowing in other arteries occurred in 13%, and the remaining patients were presumed to have large or small vessel vasospasm. The mortality rate for the entire group was 0.8%. When repeat angioplasty was applied to patients with restenosis, over 80% of the group improved at an average follow-up time of 21 months. Symptomatic restenosis may occur less often when higher balloon inflation pressures are used during PTCA.
Angioplasty, Balloon↗
Chest pain and "normal" coronary arteries--role of small coronary arteries.
To study the mechanism of chest pain in patients with insignificant epicardial coronary artery disease, 50 patients underwent great cardiac vein (GCV) flow, oxygen content and lactate determinations at rest and during pacing, and left ventricular end-diastolic pressure (LVEDP) measurements at rest and after pacing. Twenty-four patients having typical chest discomfort during pacing demonstrated significantly lower increase in flow from baseline (36 +/- 18% versus 86 +/- 24%, p less than 0.001) and decrease in coronary resistance (-17 +/- 12% versus -43 +/- 7%, p less than 0.001) compared with 26 patients without pacing-induced chest pain, despite no significant difference in myocardial oxygen consumption (MVO2) between the 2 groups. Lactate consumption at a heart rate (HR) of 150 beats/min was significantly less (28.3 +/- 21.5 versus 51.3 +/- 35.8 mM X ml/min, p less than 0.001) and the increase in LVEDP from rest to after pacing was significantly greater (5 +/- 2 versus 1 +/- 2 mm Hg, p less than 0.001) in the chest pain group. After administration of ergonovine, 0.15 mg intravenously, to 46 of these patients, 31 had typical pain either at rest (1 patient) or during pacing. This group had significantly lower increase in flow (38 +/- 20% versus 107 +/- 38%, p less than 0.001), and decrease in coronary resistance (-16 +/- 12% versus -45 +/- 11%, p less than 0.001) compared with the 15 patients not having chest pain, despite no significant difference in MVO2 between the 2 groups. Patients with chest pain also had lower lactate consumption at a HR of 150 beats/min (39.2 +/- 23.6 versus 65.3 +/- 46.3 mM X ml/min, p less than 0.01), greater arterial-GCV oxygen difference (12.5 +/- 1.3 versus 11.6 +/- 1.0 ml O2/100 ml, p less than 0.05), and a more marked increase in LVEDP from rest to after pacing (11 +/- 3 versus 5 +/- 2 mm Hg, p less than 0.001). Quantitative coronary arteriography demonstrated no significant luminal narrowing of the epicardial coronary arteries in response to ergonovine. These data are consistent with the hypothesis that some patients with chest pain and angiographically normal epicardial coronary arteries have dynamic abnormalities of the small coronary arteries or coronary microcirculation that cause abnormal vasodilator reserve or vasoconstriction, resulting in myocardial ischemia and angina pectoris.
Adult↗
Dynamic coronary obstruction as a cause of angina pectoris: implications regarding therapy.
The strong link demonstrated at autopsy between coronary atherosclerosis and angina pectoris led to the important concept that a fixed obstruction of 1 or more coronary arteries was the pathophysiologic cause of angina: myocardial ischemia and angina occurred when myocardial oxygen demand out-stripped the capacity of the diseased coronary artery to deliver oxygen. Therapeutic strategies were based on attempts to lower myocardial oxygen needs induced by physical and emotional stress. However, the finding that dynamic increases in coronary vascular resistance can also either precipitate ischemia or reduce the threshold of myocardial oxygen consumption (MVO2) at which it occurs has profoundly altered our understanding of the pathophysiologic features of angina and, therefore, its treatment. Dynamic coronary obstruction can occur at the large-vessel level, causing Prinzmetal's or variant angina. It is also possible that in some patients a continuum of large-vessel coronary vasoconstrictor tone exists, causing the common clinical situation manifested by angina with variable thresholds of onset. Recent studies have demonstrated that increases in the resistance offered to flow by small coronary arteries too small to be imaged by angiography can also decrease anginal threshold. The fact that ischemia can be precipitated by dynamic increases in large- or small-vessel coronary resistance has important implications for the therapy of angina pectoris. In those persons who mostly have a dynamic component contributing to their coronary obstruction, primary intervention with vasodilator therapy, including nitrates and calcium-channel blocking agents, are probably most effective therapeutically.(ABSTRACT TRUNCATED AT 250 WORDS)
Angina Pectoris↗
Combination therapy with calcium-channel blockers and beta blockers for chronic stable angina pectoris.
Combination therapy using calcium-channel blockers and beta blockers in patients with refractory chronic stable angina has gained much popularity, but remains highly controversial because of the potential for serious additive deleterious hemodynamic or electrophysiologic reactions. In studies involving patients with preserved left ventricular function receiving chronic oral beta blockers, short-term administration of intravenous verapamil has been shown to cause a further lowering in heart rate and blood pressure while prolonging atrioventricular node conduction; additive cardiodepressant effects were noted, including a tendency toward increased left and right heart filling pressures. Nifedipine, on the other hand, when added acutely to beta blockers, causes an increase in heart rate, a decrease in blood pressure and either no change or a slight improvement in most cardiac performance variables. Controlled, double-blind clinical trials have demonstrated that combinations of calcium-channel blockers and beta blockers result in augmented symptom benefit compared with either drug class alone. The predominant mechanism responsible for such improvement is increased lowering of myocardial oxygen demand by virtue of additive diminution in heart rate, blood pressure and, consequently, pressure-rate product both at rest and during exercise. Verapamil (and possibly diltiazem) plus beta blockers appears to have the greatest therapeutic efficacy but also the highest frequency of harmful adverse cardiac effects, whereas nifedipine plus beta blockers is generally safer but also less efficacious. Factors that should be carefully considered by clinicians contemplating combination therapy are the choice of calcium-channel blocker, the dose of calcium-channel blocker and beta blocker, the presence of antecedent left ventricular dysfunction or conduction system disease and the possibility of drug interactions. Concomitant calcium-channel blocker and beta-blocker therapy is an important contribution to the pharmacologic management of resistant patients who remain symptomatic during single drug treatment. However, the possibility of additive adverse cardiac effects mandates careful patient selection and close clinical monitoring.
Adrenergic beta-Antagonists↗
Use of calcium-channel blocking drugs in hypertrophic cardiomyopathy.
Verapamil exerts a wide spectrum of hemodynamic effects in patients with hypertrophic cardiomyopathy (HC), and its administration offers an important alternative to beta-receptor blocker therapy in such patients. The intravenous administration of verapamil to 62 patients in the catheterization laboratory decreased systolic blood pressure from 118 +/- 17 to 102 +/- 17 mm Hg (p less than 0.001). It had no significant effect on heart rate, mean pulmonary artery wedge pressure, left ventricular (LV) end-diastolic pressure or cardiac output; however, LV outflow gradient in the basal state decreased from 62 +/- 34 to 29 +/- 34 mm Hg (p less than 0.05). These findings demonstrate a decrease in LV outflow tract obstruction. Radionuclide angiography indicated the major action responsible for the reduction in obstruction appears to be an improvement in LV diastolic function. Short-term nifedipine administration to patients with HC produced no significant effect on LV outflow tract gradients and early diastolic filling. Short-term double-blind studies showed that verapamil improved exercise time by 26 +/- 35% (p less than 0.005) compared with placebo, whereas propranolol improved it by 21 +/- 35% (p less than 0.025). In a separate study, verapamil improved exercise duration by 38 +/- 58% (p = 0.02) compared with placebo, whereas nifedipine improved it by 20 +/- 47% (difference is not significant). Verapamil resulted in a more beneficial subjective symptomatic response than propranolol or nifedipine when compared with placebo. Long-term verapamil therapy was instituted in 227 patients; 133 of these patients have continued taking the medication for an average of 25 +/- 13 months because their quality of life improved compared with what they experienced with their former therapy (usually beta blocker). Improved exercise capacity of 40% has been maintained in 32 patients for 2 years. A decrease in ventricular septal thickness of 1.5 +/- 2.6 mm was also found in 32 patients studied after 39 +/- 8 months of verapamil therapy. Nine patients died during follow-up study, but it is unclear whether the drug increased survival or, conversely, whether any of the deaths could be attributed to verapamil administration. Significant adverse electrophysiologic and hemodynamic effects were seen in 59 instances. The electrophysiologic events, atrioventricular block and sinus arrest, were definitely verapamil-related, but it is uncertain how many of the hemodynamic problems of hypotension and pulmonary congestion were drug-related.(ABSTRACT TRUNCATED AT 400 WORDS)
Adolescent↗