bluuebunny/crossref_metadata_2025 huggingface dataset:
The dependence of the cardiac effects of nifedipine on the responses of the peripheral vascular system.
Authors: Kurnik P B , Tiefenbrunn A J , Ludbrook P A
Published: June 2011

To elucidate the mechanisms of reduction of left ventricular end-diastolic pressure by nifedipine in certain individuals, we evaluated cardiac and peripheral hemodynamic responses in 32 patients after they were randomly assigned to nifedipine (20 mg sublingually) or to placebo treatment. Forearm plethysmography was performed during cardiac catheterization with micromanometers. No hemodynamic parameters were changed after placebo. Left ventricular end-diastolic pressure declined by 14% (p less than .02) after nifedipine in patients with impaired left ventricular function, but was unchanged in those with normal function; indexes of peripheral venous hemodynamics (forearm venous tone, forearm volume change) were not affected. In those patients with abnormal left ventricular function, forearm vascular resistance decreased 36% and forearm blood flow increased 31% (p less than .0005 for both), while neither changed in those with normal function. Cardiac output increased by 10% in patients with impaired left ventricular function but was unchanged in the remainder, while calculated total systemic resistance fell by 24% in those with abnormal left ventricular function (p less than .002 for both). Thus, reduction of left ventricular preload by nifedipine is not attributable to venous pooling, but rather this beneficial effect appears to be attributable to improved left ventricular systolic function in response to afterload reduction, particularly in patients with impaired left ventricular function.
Rethrombosis after reperfusion with streptokinase: importance of geometry of residual lesions.
Authors: Harrison D G , Ferguson D W , Collins S M , Skorton D J , Ericksen E E , Kioschos J M , Marcus M L , White C W
Published: June 2011

We tested the hypothesis that lesion rethrombosis after streptokinase reperfusion is related to luminal size of the residual stenosis. Two independent techniques of analyzing coronary angiograms, quantitative coronary angiography and computer-based videodensitometry, were used to estimate the size of the residual lumen immediately after discontinuation of streptokinase. These techniques were selected because they provide independent estimates of cross-sectional area of a lesion with high degrees of reproducibility and minimal observer variability. Twenty-four patients who had undergone successful reperfusion with streptokinase were studied. Seven patients had lesion rethrombosis documented either on a repeat angiogram, at autopsy, or, in one case, by the fact that the patient had an acute transmural infarction resulting in death. Vessel patency was documented by repeat coronary angiography 8 to 14 days after initial streptokinase reperfusion in the other 17 patients. As assessed by quantitative coronary angiography, seven of 13 patients (54%) with minimal luminal cross-sectional areas of less than 0.4 mm2 had rethrombosis. None of the 11 patients with lumens greater than 0.4 mm2 had rethrombosis. In the 17 patients with vessels that remained patent the size of the residual lesion at repeat catheterization was compared with its size immediately after reperfusion with streptokinase. Over the intervening 8 to 14 day interval, an average percentage increase in minimal cross-sectional area of 116 +/- 34% was observed. In seven patients minimal luminal cross-sectional area more than doubled. Integrated optical density, an index of the severity of coronary stenosis derived from computer-based videodensitometry, was also useful in identifying a subgroup of patients at high risk for rethrombosis of lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
The value of lesion cross-sectional area determined by quantitative coronary angiography in assessing the physiologic significance of proximal left anterior descending coronary arterial stenoses.
Authors: Harrison D G , White C W , Hiratzka L F , Doty D B , Barnes D H , Eastham C L , Marcus M L
Published: June 2011

The results of previous work from this laboratory have shown a poor correlation between percent stenosis (determined visually with calipers) and the coronary reactive hyperemic response (an index of maximal coronary vasodilator capacity) determined during cardiac surgery. This study was performed to determine whether other parameters of lesion severity could predict the reactive hyperemic response and thus the hemodynamic significance of coronary stenoses in human beings. Twenty-three patients with lesions in the proximal left anterior descending coronary artery were studied. To account for differences in expected vessel size, patients with large diagonal branches (greater than one-half the diameter of the left anterior descending artery) arising before the lesion were excluded. Computer-assisted quantitative coronary angiography was used to measure percent diameter stenosis, percent area stenosis, and minimal stenosis cross-sectional area. With a pulsed Doppler velocity probe, reactive hyperemic responses were recorded after a 20 sec coronary occlusion of the left anterior descending artery at cardiac surgery before cardiopulmonary bypass and were quantified by the peak/resting velocity ratio (normal greater than 3.5:1). Percent area stenosis ranged from 7% to 54% for vessels with normal reactive hyperemic responses and from 27% to 94% for vessels with abnormal reactive hyperemic responses. With both percent diameter stenosis and percent area stenosis there was substantial overlap between vessels with normal and abnormal reactive hyperemic responses. In contrast, nine of nine vessels with normal reactive hyperemic responses had lesion minimal cross-sectional areas of greater than 3.5 mm2 and 13 of 14 vessels with abnormal reactive hyperemic responses had minimal cross-sectional areas of less than 3.5 mm2.(ABSTRACT TRUNCATED AT 250 WORDS)
Intra-atrial reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog.
Authors: Allessie M A , Lammers W J , Bonke I M , Hollen J
Published: June 2011

In the isolated blood-perfused canine heart we produced episodes of rapid atrial flutter by continuous infusion of acetylcholine and rapid pacing. The spread of excitation during atrial flutter was mapped with the aid of two endocavitary mapping electrodes containing 960 leads and recording from 192 different sites simultaneously. The flutter maps clearly showed that intra-atrial reentry was the mechanism responsible for the arrhythmia. However, the localization and size of the intra-atrial circuits differed from case to case even in the same heart. The orifices of the venae cavae or the atrioventricular ring did not serve as a central anatomic obstacle for circus movement. We also failed to identify a special role of the internodal pathways in the formation of the loop. Instead, the intra-atrial circuits could be found everywhere, provided sufficient atrial mass was available to accommodate the circuit. The diameter of the circuits varied between 1.5 and 3 cm at a cycle length between 65 and 155 msec. The average conduction velocity of the circulating impulse varied between 60 and 80 cm/sec. Spontaneous termination of atrial flutter frequently occurred and was based on local conduction block in a narrow part of the circuit. Another interesting aspect of these studies is the finding that during continuous circus movement of the impulse, the amount of myocardium that is activated may vary considerably. This marked periodicity in excited tissue mass during atrial flutter could adequately explain the continuously undulating baseline or typical sawtoothlike F waves as seen in the surface electrocardiogram during atrial flutter.
Reflex constriction of significant coronary stenosis as a mechanism contributing to ischemic left ventricular dysfunction during isometric exercise.
Authors: Brown B G , Lee A B , Bolson E L , Dodge H T
Published: June 2011

To study the mechanisms of myocardial ischemia during isometric exercise, handgrip was sustained, for 4.5 min at 25% of maximum by 11 patients with at least one significant coronary stenosis each, during cardiac catheterization. After recovery, the handgrip that was repeated with simultaneous infusion of nitroglycerin (50 micrograms over 4 min) directly into the diseased vessel. The cardiovascular response was assessed by hemodynamic and by computer-assisted measurements of stenosis. During the first handgrip test pulmonary capillary wedge pressure rose 56% (15 to 23 mm Hg; p less than .001), the heart rate-systolic pressure product rose 33% (p less than .01), and the diseased epicardial arteries constricted. Luminal area in the stenotic segment was reduced by 35% (p less than .01), resulting in a 243% increase in estimated stenotic flow resistance (30 to 103 mm Hg/ml/sec; p less than .001). During handgrip with intracoronary nitroglycerin, the pressure-rate product again increased 33%, but relative to resting control, capillary wedge pressure fell 4 mm Hg in association with a 32% increase in luminal area of the stenosis and a 28% reduction in flow resistance (all significantly different from the response to handgrip alone: p less than .001, .01, and .005, respectively). Thus, coronary vasoconstriction, not increased pressure-rate product, is the dominant mechanism for ischemic left ventricular dysfunction during isometric exercise in patients with significant coronary stenoses.
A prospective comparison of triple extrastimuli and left ventricular stimulation in studies of ventricular tachycardia induction.
Authors: Morady F , DiCarlo L , Winston S , Davis J C , Scheinman M M
Published: June 2011

One hundred and one patients with sustained unimorphic ventricular tachycardia underwent programmed ventricular stimulation with one of two protocols. Fifty patients underwent programmed stimulation with protocol A, which consisted of burst overdrive pacing, single, double, and triple extrastimuli at the right ventricular apex, right ventricular outflow tract, or septum, and then at the left ventricular apex. Fifty-one patients underwent programmed stimulation with protocol B, which consisted of burst overdrive pacing, single and double extrastimuli at the right ventricular apex, right ventricular outflow tract or septum, and at the left ventricular apex, followed by triple extrastimuli at these sites. The stimulation protocol was continued until sustained ventricular tachycardia or rapid, polymorphic ventricular tachycardia greater than 10 sec in duration was induced. With protocol A, clinical and nonclinical ventricular tachycardia was induced in 76% and 36% of patients, respectively; with protocol B, clinical and nonclinical ventricular tachycardia was induced in 85% and 38% of patients, respectively. Direct-current countershock for sustained polymorphic ventricular tachycardia was required in 10% of patients studied under protocol A, compared with in 2% of patients studied under protocol B. With protocol A, near-maximal yield of induced clinical (72%) and nonclinical ventricular tachycardia (30%) was attained after the use of triple extrastimuli at the first stimulation site. The yield of stimulation at a second right ventricular site and of left ventricular stimulation was only an additional 2% each. With protocol B, triple extrastimuli increased the yield of induced clinical ventricular tachycardia from 61% to 85%.(ABSTRACT TRUNCATED AT 250 WORDS)
Minoxidil in patients with chronic left heart failure: contrasting hemodynamic and clinical effects in a controlled trial.
Authors: Franciosa J A , Jordan R A , Wilen M M , Leddy C L
Published: June 2011

Minoxidil, a potent predominant arterial dilator, improves hemodynamics over the short term in patients with heart failure. In random double-blind fashion 17 patients with chronic left heart failure were given minoxidil (nine patients) or placebo (eight patients) in addition to digoxin and diuretics for 3 months. Cardiac index and heart rate increased and mean arterial pressure and systemic vascular resistance fell within 4 hr of minoxidil administration. Right heart and pulmonary arterial pressures were unchanged over the short term but rose after long-term minoxidil. After 3 months of minoxidil treatment, systemic vascular resistance was still reduced (11.7 +/- 6.3[SD] vs 17.1 +/- 3.1 U at baseline; p less than .05). Hemodynamics were similar at baseline and remained unchanged during placebo treatment. Mean left ventricular ejection fraction rose from 29.6 +/- 17.7% to 42.7 +/- 22.3% (p less than .05) after 3 months of minoxidil treatment (this result was influenced largely by responses in two patients), and remained unchanged (at 25.1 +/- 16.6%) after 3 months of placebo. Exercise duration and maximal oxygen uptake during exercise were unchanged during minoxidil or placebo treatment. Total clinical events, including increased need for diuretics, angina, ventricular arrhythmias, worsening heart failure, and death were all more frequent during minoxidil vs placebo administration (21 vs seven total events; p less than .01). Thus, despite improving hemodynamics and left ventricular function, long-term minoxidil administration was associated with a poorer clinical course in patients with chronic left ventricular failure. Furthermore, this experience demonstrates that improvement of left ventricular function alone cannot be reliably interpreted as proof of clinical efficacy of therapeutic interventions in patients with heart failure.
The physiology of external cardiac massage: high-impulse cardiopulmonary resuscitation.
Authors: Maier G W , Tyson G S , Olsen C O , Kernstein K H , Davis J W , Conn E H , Sabiston D C , Rankin J S
Published: June 2011

In intact chronically instrumented dogs, left ventricular dynamics were studied during cardiopulmonary resuscitation (CPR). Electromagnetic flow probes measured cardiac output and coronary blood flow, ultrasonic transducers measured cardiac dimensions, and micromanometers measured left ventricular, right ventricular, aortic, and intrathoracic pressures. The dogs were anesthetized with morphine, intubated, and fibrillated by rapid ventricular pacing. Data were obtained during manual external massage with dogs in the lateral and supine positions. Force of compression was varied from a peak intrathoracic pressure of 10 to 30 mm Hg, and compression rate was varied from 60 to 150/min. Increasing force of compression increased stroke volume up to a peak intrathoracic pressure of approximately 20 mm Hg, beyond which stroke volume remained constant or declined. Stroke volume appeared to result primarily from direct transmission of manual compression force to the heart rather than from positive intrathoracic pressure because peak cardiac or vascular pressures or the change in these pressures were consistently two to four times greater than the corresponding intrathoracic pressures during manual compression. With increasing compression rate, stroke volume remained relatively constant, and total cardiac output increased significantly: 425 +/- 92 ml/min at 60/min, 643 +/- 130 ml/min at 100/min, and 975 +/- 219 ml/min at 150/min (p less than .05). Left ventricular dimensions decreased minimally at higher manual compression rates. In four patients undergoing CPR, systolic and diastolic arterial blood pressure increased with faster compression rates, correlating well with data obtained in the dog. Dynamic coronary blood flow in canine experiments decreased to zero or negative values during compression. Antegrade coronary flow occurred primarily during noncompression periods and seemed to be related to diastolic aortic perfusion pressure; coronary flow at a compression rate of 150/min averaged 75% of control. Therefore stroke volume and coronary blood flow in this canine preparation were maximized with manual chest compression performed with moderate force and brief duration. Increasing rate of compression increased total cardiac output while coronary blood flow was well maintained. Direct cardiac compression appeared to be the major determinant of stroke volume during manual external cardiac massage.
Enalapril in patients with chronic heart failure: a placebo-controlled, randomized, double-blind study.
Authors: Sharpe D N , Murphy J , Coxon R , Hannan S F
Published: June 2011

A number of studies have shown short-term hemodynamic and symptomatic improvement in patients with congestive heart failure treated with angiotensin converting-enzyme inhibitors. The long-term efficacy of the oral long-acting converting-enzyme inhibitor enalapril remains to be established in controlled studies. We evaluated this drug in 36 patients with New York Heart Association functional class II to III heart failure who were clinically stable on digoxin and diuretic therapy. After baseline assessment of symptoms, exercise capacity, and results of echocardiographic examination and right heart catheterization, patients were randomly assigned to treatment with 5 mg enalapril twice daily (n = 18) or placebo (n = 18) in a double-blind fashion. The two groups had similar clinical, echocardiographic, and hemodynamic characteristics before treatment. After 3 months of treatment, the enalapril group showed a significant improvement as judged by subjective patient impression, functional class, and exercise duration (9.3 +/- 5.7 vs 17.6 +/- 5.6 min; p less than .001). Diuretic dosage was reduced in six patients and increased in one patient, one patient had died and another had been withdrawn from the study. In the placebo group there was no significant change with respect to patient impression, functional class, or exercise duration; diuretic dosage was increased in seven patients and four patients had died. Echocardiographic left ventricular dimensions were significantly reduced and left ventricular shortening fraction significantly increased in the enalapril group but were unchanged in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)
Combined renovascular hypertension and diabetes in rats: a new preparation of congestive cardiomyopathy.
Authors: Fein F S , Capasso J M , Aronson R S , Cho S , Nordin C , Miller-Green B , Sonnenblick E H , Factor S M
Published: June 2011

Myocardial function, electrophysiologic characteristics, and structure were studied in rats with both renovascular hypertension and streptozotocin-induced diabetes (HD). Ventricular papillary muscles from untreated rats with HD showed a marked slowing of isometric and isotonic contractions. Peak developed tension and peak shortening were preserved, except in one animal with findings of congestive heart failure. Transmembrane action potentials increased fivefold in duration. Myocardial interstitial fibrosis was frequently observed. Physiologic parameters of rats with HD treated by left nephrectomy, captopril, and insulin were very similar to those of age-matched controls. The mortality rate of rats with HD was 43% over 5 to 6 months in the first study. In a second study, spontaneously dying rats with HD were compared with those deliberately killed. A 55% mortality was observed over 7 months. Myocardial structural damage and histologic evidence of congestive heart failure were more frequent in spontaneously dying rats with HD. Combined renovascular hypertension and diabetes in rats appears to be a new preparation of congestive cardiomyopathy.
Continued high incidence of coronary artery disease at autopsy in Olmsted County, Minnesota, 1950 to 1979.
Authors: Elveback L , Lie J T
Published: June 2011

The autopsy records of all people over 30 years old who died and underwent autopsy in Olmsted County from 1950 through 1979 were reviewed (n = 5558, autopsy rate approximately 50%). The hearts of 530 subjects were reexamined for the severity of coronary artery disease and this determination was compared with the recorded grade. After both record and specimen the three major coronary arteries were graded according to percent reduction in luminal area (1 = 0 to 25%; 2 = 26% to 50%; 3 = 51% to 75%; 4 = 76% to 99%; 5 = occlusion). Grades 4 and 5 were designated as significant coronary disease (SCD), and 94% to 99% of diagnoses of SCD were confirmed on reexamination. The percentage of people with SCD increased during the period 1950 to 1969 and remained high in the 1970s. Cohort analysis showed an increase in the disease in all age groups (except in the 30- to 49-year-old group for the later decades of birth). There was no change in the prevalence of myocardial infarction scars over the study period.
Variables predictive of successful medical therapy in patients with unstable angina: selection by multivariate analysis from clinical, electrocardiographic, and angiographic evaluations.
Authors: Ouyang P , Brinker J A , Mellits E D , Weisfeldt M L , Gerstenblith G
Published: June 2011

Although unstable angina can be initially controlled with medical therapy in most patients, there is a high incidence of subsequent death, myocardial infarction, or need for coronary bypass surgery to control symptoms. Identification at the time of presentation of the patient likely to do poorly on continued medical therapy would be useful in advising consideration of surgical therapy. Since coronary arterial spasm may have a significant role in the pathophysiology of unstable angina in some patients, the recently developed calcium channel antagonists may therefore be of particular benefit in the medical therapy of unstable angina. One hundred thirty-eight patients were entered into a randomized double-blind study of the efficacy of adding nifedipine to conventional treatment of unstable angina (nitrates and beta-blockers) and were followed for 18 months. Of these patients, 104 underwent coronary arteriography. A multivariate Cox's hazard function analysis was applied to variables selected from the history, electrocardiographic (ECG) changes during chest pain, and from scintigraphic and coronary arteriographic data to determine those variables most predictive of response to medical therapy. The percentage of the left ventricular myocardium supplied by vessels with 70% or greater luminal stenosis was the most significant variable in influencing failure of medical therapy defined as sudden death, myocardial infarction, or need for bypass surgery. Whether or not the patient received nifedipine was the second most powerful variable, with the use of nifedipine reducing by half the relative risk of failing medical therapy. These were followed by cigarette smoking and presence of global ST segment changes during ischemia. After 18 months the nifedipine group had fewer patients failing medical therapy (p = .02), with fewer patients undergoing coronary bypass surgery (p less than .01). However, nifedipine did not appear to have a preventive effect against myocardial infarction or death. Kaplan-Meier actuarial curves confirmed that medical therapy was significantly less successful in the presence of increasing numbers of significantly stenotic vessels (p = .03). However, nifedipine provided a significant beneficial effect in patients with two or more stenotic vessels (p less than .01) and in whom 50% or more of the myocardium was supplied by vessels with 70% or greater stenosis (p = .01). Thus, although patients with advanced obstructive coronary disease have the greatest likelihood of unfavorable outcomes, the addition of nifedipine is of significant benefit.(ABSTRACT TRUNCATED AT 400 WORDS)
Sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy: electrophysiologic testing and lack of response to antiarrhythmic drug therapy.
Authors: Poll D S , Marchlinski F E , Buxton A E , Doherty J U , Waxman H L , Josephson M E
Published: June 2011

Eleven consecutive patients with idiopathic dilated cardiomyopathy and spontaneous, sustained ventricular tachycardia (VT) of uniform morphology underwent programmed ventricular stimulation and serial antiarrhythmic drug testing. The mean ejection fraction was 30 +/- 6.4%. Sustained VT was induced by programmed electrical stimulation in all 11 patients. A mean of 3.7 +/- 2.4 antiarrhythmic drugs were evaluated by programmed stimulation, including at least one experimental agent in eight patients. In nine of 11 patients VT remained inducible on all drug therapy. During a mean follow-up period of 21 +/- 14 months there were four sudden deaths and two patients with recurrences of VT. In all six patients with sudden death or recurrence of VT, the arrhythmia remained inducible on drug therapy. Three patients who died suddenly had a hemodynamically stable, induced tachycardia on antiarrhythmic therapy. Of eight patients treated with amiodarone, only two were successfully treated. We conclude that in patients with sustained VT and idiopathic dilated cardiomyopathy, VT can be induced by programmed electrical stimulation. VT will usually remain inducible on antiarrhythmic therapy, and sudden death can occur despite slowing and improved tolerance of the induced arrhythmia. Amiodarone may have limited efficacy, and more aggressive therapy, such as surgery or implantation of an automatic internal defibrillator, should be considered in this patient population.
Diltiazem-induced blockade of sympathetically mediated constriction of normal and diseased coronary arteries: lack of epicardial coronary dilatory effect in humans.
Authors: Hossack K F , Brown B G , Stewart D K , Dodge H T
Published: June 2011

To determine mechanisms of benefit from diltiazem, 13 patients with coronary disease performed sustained isometric handgrip exercise and repeated the procedure during intravenous infusion of diltiazem (0.25 mg/kg bolus followed by 0.003 mg/kg/min). Cardiovascular responses to handgrip, diltiazem, their combination, and nitroglycerin were assessed by hemodynamic and electrocardiographic measurements and by computer-assisted measurements of normal and diseased segments of epicardial coronary arteries. Handgrip produced increases in heart rate (12%; p less than .001), pulmonary arterial pressure (19%; p less than .005), and pulmonary wedge pressure (33%; p less than .005). Diltiazem produced significant reductions in heart rate (7%; p less than .05) and aortic pressure (14%; p less than .001). Pulmonary arterial pressure and pulmonary wedge pressure were unchanged by diltiazem. Diltiazem did not prevent the increase in heart rate or in aortic or wedge pressure associated with handgrip. Diltiazem prolonged atrioventricular conduction from 0.18 +/- 0.03 to 0.20 +/- 0.03 sec (p less than .001). Compared with control values, nitroglycerin reduced aortic pressure (14%; p less than .005), pulmonary arterial pressure (38%; p less than .001), and pulmonary wedge pressure (42%; p less than .005). Heart rate was unchanged. The constriction (20%) in lumen area of normal coronary arterial segments during handgrip was effectively prevented by infusion of diltiazem (1%; p less than .001). Nitroglycerin produced a significantly greater increase (20%) in diameter of normal coronary arterial segments than diltiazem (3%; p less than .001) and tended to have a more favorable effect than diltiazem on stenosis minimum area and flow resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
Overdrive suppression of conduction in the canine His-Purkinje system after occlusion of the anterior septal artery.
Authors: Takahashi N , Gilmour R F , Zipes D P
Published: June 2011

The purpose of these experiments was to determine whether overdrive suppression of conduction (OSC), i.e., transient worsening of conduction or development of atrioventricular block after cessation of rapid pacing, could be produced in the canine His-Purkinje system damaged by ligation of the anterior septal coronary artery and to investigate the responsible mechanism. We found that OSC occurred in vivo after rapid ventricular and His bundle pacing but not after atrial pacing, and that it occurred in vitro after rapid pacing from the left bundle branch but not after pacing from the proximal His bundle. OSC was related to the duration and cycle length of pacing. Lidocaine increased while verapamil reduced the duration of OSC in vivo. The mechanism responsible for the unidirectionality of OSC is not clear but is probably related to the geometry of the atrioventricular junction and the anterograde versus the retrograde activation sequence. Changes in regional myocardial blood flow, autonomic tone, hemodynamic variables, or ventricular function do not appear to be required to produce OSC, based on the demonstration of the phenomenon in vitro. The data suggest a time- and rate-dependent change in factors affecting conduction such as excitability or cell-to-cell coupling, possibly due to accumulation of intracellular cations such as calcium.
The abnormal exercise electrocardiogram in apparently healthy men: a predictor of angina pectoris as an initial coronary event during long-term follow-up.
Authors: McHenry P L , O'Donnell J , Morris S N , Jordan J J
Published: June 2011

A group of 916 apparently healthy men between the ages of 27 and 55 years (mean 37) were followed up with serial medical and exercise test evaluations for a period of 8 to 15 years (mean 12.7) to determine (1) the prevalence and specific types of new coronary events observed in subjects with and without abnormal ST segment responses to exercise and (2) the predictive value of a serial conversion to an abnormal ST segment response to exercise for new coronary events. During the initial evaluation there were 23 subjects (2.5%) with an abnormal ST segment response to exercise. During follow-up there were nine (39%) coronary events in this group: eight cases of angina and one of sudden death. With serial testing, an additional 38 subjects (5.1%) experienced conversion to an abnormal ST segment response to exercise. During follow-up there were 12 (32%) coronary events in this group: 10 cases of angina, one of myocardial infarction, and one other. There were 833 subjects with normal ST segment responses to exercise with all tests. In this group there were 44 (5.3%) coronary events: 25 cases of myocardial infarction, seven of sudden death, and 12 of angina. We conclude that in apparently healthy middle-aged men an abnormal ST segment response to exercise is predictive of angina pectoris but not of myocardial infarction or sudden cardiac death as an initial coronary event.
Evolution of infarct size during the early use of nifedipine in patients with acute myocardial infarction: the Norwegian Nifedipine Multicenter Trial.
Authors: Sirnes P A , Overskeid K , Pedersen T R , Bathen J , Drivenes A , Frøland G S , Kjekshus J K , Landmark K , Rokseth R , Sirnes K E
Published: June 2011

In a multicenter double-blind study, 227 patients with suspected acute myocardial infarction (AMI) were randomized within 12 hr from onset of symptoms to treatment with nifedipine (112 patients) or placebo (115 patients). AMI was confirmed in 74 patients on nifedipine and in 83 on placebo. Patients with AMI received nifedipine 5.5 +/- 2.9 hr (mean +/- SD) after onset of symptoms. Infarct size was assessed by the release of creatine kinase isoenzyme MB (CK-MB). Infarct size index (CK-MB geq/m2) was 25 +/- 16 (n = 71) in the nifedipine group and 23 +/- 13 (n = 77) in the placebo group (NS). After the first 10 mg of nifedipine systolic blood pressure fell from 147 +/- 30 to 135 +/- 28 mm Hg (p less than .01) and heart rate rose from 75 +/- 18 to 79 +/- 19 beats/min (p less than .01). No change was observed after the first placebo dose. The treatment was continued for 6 weeks. Over this period there were 10 deaths in each group. Early treatment with nifedipine in patients with AMI does not seem to reduce infarct size as determined by enzyme level.
Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation.
Authors: Yock P G , Popp R L
Published: June 2011

We evaluated the accuracy of a noninvasive method for estimating right ventricular systolic pressures in patients with tricuspid regurgitation detected by Doppler ultrasound. Of 62 patients with clinical signs of elevated right-sided pressures, 54 (87%) had jets of tricuspid regurgitation clearly recorded by continuous-wave Doppler ultrasound. By use of the maximum velocity (V) of the regurgitant jet, the systolic pressure gradient (delta P) between right ventricle and right atrium was calculated by the modified Bernoulli equation (delta P = 4V2). Adding the transtricuspid gradient to the mean right atrial pressure (estimated clinically from the jugular veins) gave predictions of right ventricular systolic pressure that correlated well with catheterization values (r = .93, SEE = 8 mm Hg). The tricuspid gradient method provides an accurate and widely applicable method for noninvasive estimation of elevated right ventricular systolic pressures.
The noninvasive localization of ventricular pacing sites by radionuclide phase imaging.
Authors: Bashore T M , Stine R A , Shaffer P B , Bush C A , Leier C V , Schaal S F
Published: June 2011

This study was designed to investigate the potential role of radionuclide angiographic phase imaging in defining ventricular pacing sites. Twenty patients were paced from multiple right ventricular and left ventricular sites. Ten patients had both normal wall motion and normal electrocardiograms (ECGs), while 10 patients had segmental wall motion abnormalities and/or bundle branch block. Both continuous pacing and premature ventricular stimuli were performed. Multiple (two to three) views of each pacing site were obtained by radionuclide angiography and the ventricular site was determined by subsequent phase imaging. Simultaneous 12-lead ECGs were also obtained. The phase-imaging technique accurately localized all 35 right ventricular and 21 of 25 (84%) left ventricular sites to a specific segment. Statistically, this localization ability was independent of baseline wall motion or conduction system disease. In addition, sites as close as 1.5 cm were identified. The 12-lead ECG distinguished left ventricular from right ventricular pacing sites in all patients. Segmental localization by ECG in the right ventricle was accurate in 24 of 35 (69%) and in the left ventricle in 17 of 25 (68%). Thus, radionuclide angiographic phase imaging provides excellent descriptive information regarding the focus of ventricular pacing ectopy and can define both sites of continuous pacing and intermittent premature ventricular stimulation. These findings provide a basis for further assessment of the role of phase imaging in the evaluation of patients with spontaneous ventricular ectopy.
Relationships between beat-to-beat interval and the strength of contraction in the healthy and diseased human heart.
Authors: Seed W A , Noble M I , Walker J M , Miller G A , Pidgeon J , Redwood D , Wanless R , Franz M R , Schoettler M , Schaefer J
Published: June 2011

Twenty-six adult patients, classified by clinical and catheter criteria into groups of those with normal and abnormal left ventricular function, were studied during cardiac catheterization. Right heart pacing was established, and left ventricular dP/dt was measured with end-catheter manometers. By varying the interval preceding a test beat after periods of steady pacing it was confirmed that recovery of left ventricular mechanical function (maximum dP/dt) occurs approximately 800 msec (optimum interval) after a beat. The augmentation of maximum dP/dt of the first 2 beats after an extrasystole, each spaced at the optimum interval, was also studied; the amount of potentiation was varied by alterations in extrasystolic interval. Potentiation decayed from the first to the second postextrasystolic beat with a ratio that was fixed in each individual patient. The ratio (recirculation fraction) was higher in patients with normal than in those with abnormal left ventricular function (mean +/- SD 0.52 +/- 0.10 vs 0.37 +/- 0.11, p less than .005). There was an inverse relationship between this ratio and the degree of potentiation of the first postextrasystolic beat (r = .80, p less than .001). We postulate a disturbance of excitation-contraction coupling mechanisms to explain these effects.
Transcutaneous oxygen tension and capillary morphologic characteristics and density in patients with chronic venous incompetence.
Authors: Franzeck U K , Bollinger A , Huch R , Huch A
Published: June 2011

The transparent oxygen electrode, recently developed by Huch and his co-workers, permits monitoring of transcutaneous oxygen tension (tcPO2) at defined sites on the capillaroscopic image obtained by videomicroscopy. This combined system has been applied to study the nutritional skin capillaries of patients with chronic venous incompetence (CVI). The results of 44 studies in 17 patients with CVI demonstrated a direct correlation between tcPO2 and density and morphologic characteristics of the superficial capillaries. The mean tcPO2 was 47.7 +/- 14.4 mm Hg at the site of incompetent perforating veins of the ankle without major trophic changes. There was no statistically significant difference between the mean values obtained in patients and control subjects (56.8 +/- 9.9 mm Hg). Videomicroscopic examination revealed dilated and tortuous capillaries surrounded by halo formations. In areas of hyperpigmentation, induration, and hyperkeratosis, significantly decreased mean tcPO2 (22.5 +/- 7.0 mm Hg; p less than .001) corresponded to reduced capillary density (less than 10 capillaries/mm2). In avascular skin areas (scar tissue, white atrophy) tcPO2 was measured at 0 mm Hg. No capillaries, or a greatly reduced number, were visible at such sites, resulting in a distance between capillary and cathode tip of the oxygen sensor of greater than 100 micron. The combined system of tcPO2 measurement and simultaneous videomicroscopy gives new pathophysiologic information on the development of skin ulcers and may be useful for the objective comparison of different therapeutic modalities at the microcirculatory level.
Magnetic resonance imaging in patients with congenital heart disease.
Authors: Higgins C B , Byrd B F , Farmer D W , Osaki L , Silverman N H , Cheitlin M D
Published: June 2011

Magnetic resonance imaging (MRI) was conducted with use of the spin-echo technique (0.35 Tesla) in 22 patients with a variety of congenital and cardiovascular anomalies and in 16 normal volunteers. Electrocardiographic (ECG) synchronization of the data acquisition produced transverse, parasagittal, and coronal tomograms that were used to define size and relationship of the great vessels and internal cardiac structures. MRI findings were corroborated by angiography and sector-scan echocardiography. In most patients the diagnosis had been established before the MRI study. MRI detected all of 11 abnormalities at the level of the great vessels, all of six atrial septal abnormalities, and 10 of 11 ventricular septal defects. Images of poor quality resulting from patient motion were obtained in the one instance in which a small ventricular septal defect was not imaged. Of two patients with Ebstein's anomaly, the displacement of the tricuspid leaflets was shown in one patient but was not evident in another. Complex anomalies such as double-outlet right ventricle, uncorrected L-transposition, single atrioventricular valve, single ventricle, and common ventricle were clearly shown by MRI. Initial experience with MRI has indicated the effectiveness of this technique for defining great vessel and internal cardiac anatomy in patients with congenital heart disease. This is accomplished without the use of contrast media and is thus a completely noninvasive technique for cardiovascular diagnosis.
Effects of a single bolus of urokinase in patients with life-threatening pulmonary emboli: a descriptive trial.
Authors: Petitpretz P , Simmoneau G , Cerrina J , Musset D , Dreyfus M , Vandenbroek M D , Duroux P
Published: June 2011

To evaluate hemodynamic, angiographic, and biological effects of a single bolus of urokinase, an open descriptive trial was conducted in a homogeneous group of 14 patients with acute life-threatening pulmonary emboli and without prior cardiopulmonary disease. For every patient the efficacy of the treatment was evaluated by comparing control and posttherapeutic values after the bolus injection of 15,000 IU/kg body weight urokinase (urinary source) administered in 10 min in the right atrium, followed by continuous intravenous full-dose heparin therapy. In two patients clinical status, hemodynamics, vascular obstruction, and biological (fibrinogen and plasminogen levels) parameters remained unchanged. One of these two patients died, making the mortality rate for the whole group 7%. Twelve of 14 patients showed rapid clinical improvement. Evaluation at 12 hr demonstrated significant decreases in pulmonary vascular obstruction (Miller index, 34%), total pulmonary vascular resistances (37%), and fibrinogen and plasminogen levels (41% and 40%, respectively), without any significant change in cardiac index. The hemodynamic sequential measurements performed (1,3, 6, and 12 hr) in seven of the 12 improved patients showed that the greatest percentage of the total hemodynamic improvement occurred within the first 3 hr after bolus administration of urokinase. No severe hemorrhagic complications were observed. Because of its rapid efficacy and its low cost, the bolus technique appeared particularly useful in the treatment of patients with acute life-threatening pulmonary emboli.
Coronary thrombolysis with recombinant human tissue-type plasminogen activator: a prospective, randomized, placebo-controlled trial.
Authors: Collen D , Topol E J , Tiefenbrunn A J , Gold H K , Weisfeldt M L , Sobel B E , Leinbach R C , Brinker J A , Ludbrook P A , Yasuda I
Published: June 2011

Forty-five patients with acute transmural myocardial infarction and angiographically confirmed complete coronary occlusion were prospectively randomized, two for one, to treatment of acute coronary thrombosis with intravenous recombinant human tissue-type plasminogen activator (rt-PA) or placebo. Each of five additional consecutive patients was treated with a high dose of rt-PA for 2 hr. Twenty-five of 33 patients (75%) receiving 0.5 to 0.75 mg/kg of rt-PA over 30 to 120 min had angiographically proven recanalization within 90 min of initiation of therapy. Only one of 14 patients given placebo had spontaneous recanalization within 45 min (p less than .001). Thirteen placebo-treated patients were crossed over to the intracoronary rt-PA group. Nine (69%) exhibited subsequent recanalization within 45 min. Levels of circulating fibrinogen decreased after treatment with rt-PA by an average of only 8% of baseline values. None of the patients manifested a depletion of fibrinogen level to below 100 mg/dl. Six patients who were completely unresponsive to rt-PA were subsequently treated with intracoronary streptokinase and none responded. Thus, either intravenous or intracoronary rt-PA induced coronary thrombolysis without eliciting clinically significant fibrinogenolysis in patients with evolving myocardial infarction due to thrombotic coronary occlusion.
Efficacy of left cardiac sympathectomy in the treatment of patients with the long QT syndrome.
Authors: Bhandari A K , Scheinman M M , Morady F , Svinarich J , Mason J , Winkle R
Published: June 2011

Ten patients with the long QT syndrome and recurrent syncope and/or cardiac arrest caused by ventricular arrhythmias underwent left stellate (one patient) or left cervicothoracic sympathectomy (nine patients) after failing to respond to high-dose beta-blocker therapy. The syndrome was familial in four and idiopathic in six. All patients had a prolonged resting QT interval (548 +/- 51 msec, mean +/- SD) and corrected QT interval (QTc) (556 +/- 43 msec). After sympathectomy the mean QTc shortened significantly from 556 +/- 43 to 508 +/- 65 msec (p less than .05) but the QTc remained abnormal in all but one patient. Over a mean follow-up period of 38.6 +/- 19 months, eight patients developed recurrent symptoms that included cardiac arrest in three (one fatal, two nonfatal), syncope in four, and presyncope in six. The addition of beta-blockers was ineffective in suppressing the recurrent symptoms. The control of symptoms required more extensive sympathectomy (three patients), chronic atrial pacing (three patients), and implantation of an automatic internal defibrillator (one patient). Only one patient has remained asymptomatic without drug or pacemaker therapy. In conclusion, left cervicothoracic sympathectomy proved inadequate for long-term control of symptoms in most patients with the long QT syndrome. These patients usually required concomitant drugs, more extensive surgery, or long-term cardiac pacing for symptomatic relief.
Catheter ablation of the atrioventricular junction: a report of the percutaneous mapping and ablation registry.
Authors: Scheinman M M , Evans-Bell T
Published: June 2011

An international registry was formed to collate data for patients undergoing attempted catheter ablation of the atrioventricular (AV) junction and insertion of a permanent pacemaker. Over the past 2 years, data was submitted for 127 patients who were followed for a mean of 9.9 +/- 8.2 months. The most common arrhythmia treated was chronic or paroxysmal atrial fibrillation or flutter (78 patients, 61%); the remainder had supraventricular tachycardia due to AV node reentry, ectopic atrial tachycardia, or incorporated an accessory pathway. A single shock of 150 to 400 J was effective in producing chronic third-degree AV block in 45 patients while two or more shocks were used in an additional 45 patients. There was no significant difference in the total cumulative energy used in successful and unsuccessful procedures. Immediate complications related to the shock included ventricular fibrillation (one patient), pericardial tamponade (one patient), and transient hypotension (one patient). No chronic sequelae occurred as a result of these complications. Late complications (1 day to 1 month) included ventricular tachycardia (three patients), sepsis involving the pacemaker pocket (two patients), staphylococcal sepsis from temporary pacing catheter (one patient), thrombophlebitis (one patient), thrombosis of the left subclavian vein (one patient), and hemothorax (one patient). Follow-up evaluation revealed chronic third degree AV block in 90 (71%) and AV conduction resumed but no drugs were required for arrhythmia control in eight (6.5%) and arrhythmia control was achieved with previously ineffective drugs in 16 (13%). Thirteen patients (10%) had no improvement and five of these patients underwent cardiac electrosurgery for direct His bundle ablation.(ABSTRACT TRUNCATED AT 250 WORDS)
Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone.
Authors: Monrad E S , McKay R G , Baim D S , Colucci W S , Fifer M A , Heller G V , Royal H D , Grossman W
Published: June 2011

To elucidate the mechanisms by which the new bipyridine inotropic agent milrinone improves cardiac function, we examined multiple indexes of left ventricular diastolic function before and after administration of milrinone to patients with advanced (NYHA class III or IV) congestive heart failure. In 13 patients left ventricular pressure measurements were made with a micromanometer to permit assessment of peak negative dP/dt and the time constant of left ventricular isovolumic relaxation, T, before and after milrinone. In nine patients radionuclide ventriculographic studies were performed during left heart catheterization, allowing calculation of left ventricular peak filling rate, volumes, and the diastolic pressure-volume relationship before and after milrinone. After intravenous administration of milrinone, peak negative dP/dt increased (+ 18%; p less than .01) and T decreased (-30%; p less than .01), while heart rate increased by only 8% (87 +/- 12 to 94 +/- 15 beats/min; p less than .01), left ventricular systolic pressure did not change, and mean aortic pressure fell by 11% (p less than .01). Left ventricular peak filling rate increased (1.2 +/- 0.6 to 1.7 +/- 0.7 end-diastolic volumes/sec; p less than or equal to .02) despite a decrease in left ventricular filling pressure (mean pulmonary wedge pressure 27 +/- 7 to 18 +/- 9 mm Hg; p less than .01). There was a fall in left ventricular end-diastolic pressure (28.6 +/- 6 to 19 +/- 7 mm Hg; p less than or equal to .01), with no significant change in left ventricular end-diastolic volume. This was associated with a downward shift in the left ventricular diastolic pressure-volume relationship in most cases.(ABSTRACT TRUNCATED AT 250 WORDS)