bluuebunny/crossref_metadata_2025 huggingface dataset:
Venous responses to salt loading in hypertensive subjects.
Authors: Takeshita A , Ashihara T , Yamamoto K , Imaizumi T , Hoka S , Ito N , Nakamura M
Published: June 2011

It has been previously suggested that salt loading produces structural changes of the arteries in hypertensive patients who respond to salt loading with a greater rise of blood pressure. This study examined the possibility that salt loading alters venous distensibility in hypertensive patients. Twenty-one patients with essential hypertension were placed on a low-sodium diet (70 meq) for 7 days and then were placed on a high-sodium diet (345 meq) for 7 days. Patients were arbitrarily divided into two groups based on the response of their blood pressure to salt loading: (1) those whose mean blood pressure increased by more than 10% while on the high-salt diet as compared with those on the low-salt diet (salt-responsive patients, n = 8) and (2) those whose mean blood pressure did not increase by more than 10% (salt-nonresponsive patients, n = 13). The venous pressure-volume relationship was determined in the forearm with a water-filled plethysmograph when patients were on the low- and high-salt diet. Venous pressure-volume curves were not different between salt-responsive and salt-nonresponsive patients while on the low-salt diet. High-salt intake shifted the curve toward the pressure axis for salt-responsive patients (p less than .05) but not for salt-nonresponsive patients. Phentolamine, 1 mg administered intravenously for 5 min, did not significantly alter venous pressure-volume curves for either group while on the low- or high-salt diet. These results suggest that salt loading decreased venous distensibility in salt-responsive patients, which resulted from nonadrenergic mechanisms: structural changes of the veins could perhaps be included as one of these mechanisms.
Bayesian analysis of data from radionuclide angiocardiograms for diagnosis of coronary artery disease.
Authors: Christopher T D , Konstantinow G , Jones R H
Published: June 2011

A continuous Bayesian model was developed by fitting a beta-function to the frequency distributions of resting ejection fraction, exercise ejection fraction, and change in end-systolic volume during exercise measured by radionuclide angiocardiography in a group of 249 men with coronary artery disease (CAD) and in a group of 56 men without disease. This model, then prospectively applied to 250 men with chest pain, did not increase the overall accuracy of the test but did increase the diagnostic content for individual patients. The diagnostic efficacy of the continuous Bayesian model was compared with previously determined optimal discrete criteria of a positive or negative test. Patients with CAD showed a maximum and mean increase in probability of disease of +0.58 and +0.11, respectively, by the continuous Bayesian model and +0.14 and +0.05, respectively, by discrete criteria. Men without significant disease showed a maximum and mean decrease in probability of disease of -0.73 and -0.38, respectively, by Bayesian analysis and -0.36 and -0.27, respectively, by optimal discrete criteria. Moreover, all 29 patients who died during a 35 month interval after study had a probability of CAD of 0.95 or greater by the continuous Bayesian model. These findings indicate that Bayesian analysis of radionuclide angiocardiographic test results with continuous distributions of left ventricular function measurement enhances the diagnostic and prognostic information for individual patients with symptoms suggestive of CAD.
Noninvasive evaluation of the ratio of pulmonary to systemic flow in atrial septal defect by duplex Doppler echocardiography.
Authors: Kitabatake A , Inoue M , Asao M , Ito H , Masuyama T , Tanouchi J , Morita T , Hori M , Yoshima H , Ohnishi K
Published: June 2011

The ratio of pulmonary to systemic flow (Qp/Qs) was noninvasively evaluated by duplex Doppler echocardiography in 22 patients with atrial septal defects (ASDs). Right and left ventricular stroke volumes (RSV, LSV) were determined from the recordings of ejection blood flow velocity and diameter at the level of the pulmonary and aortic orifices in each ventricular outflow tract. The ratio RSV/LSV, determined by the duplex Doppler echocardiography, was compared with Qp/Qs by oximetry. The RSV/LSV for 10 normal subjects was 0.99 +/- 0.05 (mean +/- SD), whereas the RSV/LSV for patients with ASD, 2.26 +/- 0.63, was significantly higher than that for normal subjects (p less than .01). In patients with ASD, a fairly good correlation was found between RSV/LSV and Qp/Qs (r = .92, p less than .01; y = 1.11x - 0.30), and this high correlation was found even in patients with complications such as pulmonary hypertension, mitral and tricuspid regurgitation, Eisenmenger complex, and ventricular septal defect. We also found that semilunar valve regurgitation modified the value of RSV/LSV in accordance with the degree of regurgitation. These findings indicate that, with a few limitations, the Doppler index RSV/LSV is clinically useful in the estimation of the magnitude of the shunt flow in patients with ASD and that the limitations could be overcome by additional Doppler examination.
Prosthetic valve endocarditis.
Authors: Ivert T S , Dismukes W E , Cobbs C G , Blackstone E H , Kirklin J W , Bergdahl L A
Published: June 2011

Fifty-three (3.6%; actuarially 4.1% at 48 months) of 1465 consecutive in-hospital survivors of valve replacement from 1975 to July 1979 (aortic, mitral, or aortic and mitral, only one untraced) developed prosthetic valve endocarditis (PVE). Incremental risk factors for developing PVE were native valve endocarditis (p less than .0001), black race (p = .0001), mechanical prosthesis (vs bioprosthesis) (p = .005), male sex (p = .04), and longer cardiopulmonary bypass time (p = .09). In general, the hazard function for developing PVE was greatest at 3 weeks after valve replacement. Patients with native valve endocarditis had a tendency to develop PVE early after valve replacement, as did patients in whom mechanical prostheses were used. PVE associated with Staphylococcus epidermidis tended to appear within 6 months of valve replacement, whereas streptococcal PVE tended to appear later after valve replacement. PVE took an atypical form in some patients, but patients with possible PVE (n = 6) had the same findings as those with certain PVE (n = 47). In 11 patients bacteriologic confirmation of PVE was not obtained. The typical prosthetic and periprosthetic characteristics of PVE were present in 30 of the 40 cases in which observations were possible. PVE is a serious condition; 34 (64%) of our 53 patients died. Most deaths occurred within 3 months of the first evidence of PVE. Recovery of some patients is possible with appropriate medical and surgical treatment, but more intense preventive measures are indicated.
Recordings of basal ventricular preexcitation from electrode catheters in patients with accessory atrioventricular connections.
Authors: Mitchell L B , Mason J W , Scheinman M M , Winkle R A , Burchell H B
Published: June 2011

To determine the effects of ventricular preexcitation via accessory atrioventricular connections (ACs) on the sequence of basal ventricular activation, electrophysiologic study records of 22 patients with AC were reviewed. In each, AC site was confirmed by mapping done at operation. Local ventricular preexcitation (VP), defined as earlier timing of a local ventricular electrogram relative to the surface electrocardiographic QRS onset in preexcited compared with in normal QRS complexes, was assessed at the coronary sinus and at the ventricular septal summit recorded from the His bundle site. Five patients with concealed AC did not have VP. VP patterns with manifest AC were similar during average fusion QRS complexes and maximum ventricular preexcitation. Left free wall and left crux AC produced VP apparent on the ventricular electrogram recorded at the coronary sinus alone. With anteroseptal AC, VP was noted only at the ventricular septal summit. Posteroseptal AC produced VP that was apparent on the ventricular electrogram recorded at the coronary sinus and on the electrogram of the ventricular septal summit. Right free wall AC preexcited neither of these basal ventricular regions. The observation of VP patterns may help in localizing AC and may be particularly useful in patients without retrograde AC function at electrophysiologic study.
The relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality in the 2 years after myocardial infarction.
Authors: Bigger J T , Fleiss J L , Kleiger R , Miller J P , Rolnitzky L M
Published: June 2011

We examined the relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality after the occurrence of myocardial infarction in 766 patients who enrolled in a nine-hospital study and underwent two special tests. Frequency and repetitiveness of ventricular premature depolarizations (VPDs) were determined by computer analysis of predischarge 24 hr electrocardiographic recordings. The left ventricular ejection fraction (LVEF) was determined by radionuclide ventriculography and dichotomized at its optimal value of 30%. Frequency of VPDs was divided into three categories: (1) less than one per hour, (2) one to 2.9 per hour, and (3) three or more per hour. Repetitiveness of VPDs was also divided into three categories: (1) no repetitive VPDs, (2) paired VPDs, and (3) VPD runs. These variables were related, one at a time and jointly, to total mortality and to deaths caused by arrhythmias. The hazard ratios for dying in the higher or highest risk stratum vs the lower or lowest stratum for each variable (adjusted for the effects of the others) were: LVEF below 30%, 3.5; VPD runs, 1.9; and VPD frequency of three or more per hour, 2.0. There were no significant interactions among the three variables with respect to effects on the risk of mortality. There was a suggestion of an interaction between each risk variable and time after infarction. LVEF below 30% was a better predictor of early mortality (less than 6 months) and the presence of ventricular arrhythmias was a better predictor of late mortality (after 6 months).(ABSTRACT TRUNCATED AT 250 WORDS)
Clinical efficacy and electrophysiologic effects of encainide in patients with Wolff-Parkinson-White syndrome.
Authors: Prystowsky E N , Klein G J , Rinkenberger R L , Heger J J , Naccarelli G V , Zipes D P
Published: June 2011

We performed electrophysiologic studies in 19 patients with accessory pathways before and during encainide therapy with a mean daily dose of 197 mg. Fourteen patients had manifest accessory atrioventricular connections, and five patients had concealed accessory atrioventricular connections. The patients had recurrent atrioventricular reentrant tachycardia for a mean of 15.8 years and had received a mean of 3.6 drug trials without successful suppression of recurrent arrhythmias. Encainide caused complete antegrade conduction block in the accessory pathway in eight of 14 patients with manifest accessory atrioventricular connections. The shortest atrial pacing cycle length maintaining 1:1 conduction over the accessory pathway at control study w3as 328 +/- 66 msec in patients in whom antegrade conduction block occurred, and it was 247 +/- 21 msec (p less than .01) in patients in whom conduction remained during encainide therapy. Retrograde conduction over accessory atrioventricular connections could be evaluated in 14 patients, and complete block occurred in seven patients during encainide therapy. There was no correlation between control retrograde effective refractory period or conduction of the accessory pathway and subsequent development of conduction block with encainide therapy. It should be noted that five patients who developed drug-related retrograde block over the accessory pathway had initial retrograde effective refractory periods for the accessory pathway less than 270 msec. Nineteen patients had atrioventricular reentrant tachycardia initiated at control electrophysiologic study. Encainide prevented induction of tachycardia in 10 patients, and in the other nine patients, cycle length of tachycardia increased during drug treatment from 313.9 +/- 53.1 to 418.3 +/- 80.9 msec (p less than .001), primarily due to an increase in ventriculoatrial conduction time from 162.2 +/- 43.8 to 238.3 +/- 87.9 msec (p less than .01). Fifteen patients continued encainide treatment for a mean of 18 months (range 7 to 38), and all but one patient remain asymptomatic. Encainide is well tolerated and prevents recurrence of reentrant tachycardia in patients with Wolff-Parkinson-White syndrome very effectively.
Comparative effect of disopyramide and ethmozine in suppressing complex ventricular arrhythmias by use of a double-blind, placebo-controlled, longitudinal crossover design.
Authors: Pratt C M , Young J B , Francis M J , Taylor A A , Norton H J , English L , Mann D E , Kopelen H , Quinones M A , Roberts R
Published: June 2011

This placebo-controlled, double-blind, longitudinal crossover study compares the efficacy of disopyramide and ethmozine, a new investigational drug, in suppressing frequent (40 or more per hour) ventricular premature depolarizations (VPDs) in 27 patients completing a 37 day protocol. Although both drugs significantly reduced VPDs relative to placebo, ethmozine was a superior antiarrhythmic drug in ach9eving near-total abolition of VPDs (30% of patients), which was never observed during disopyramide dosing (p less than .05). At the 80% VPD reduction level, ethmozine was effective in 56% of all patients compared with an effectiveness in only 22% of patients during disopyramide therapy (p less than .05). The mean peak plasma level of ethmozine was 0.66 +/- 0.8 micrograms/ml, which significantly fell to a trough level of 0.1 +/- 0.08 micrograms/ml (p less than .001). Mean peak and trough plasma levels of disopyramide exhibited less fluctuation (2.6 +/- 0.9 micrograms/ml vs 2.2 +/- 0.9 micrograms/ml). Ethmozine had no effect on the QT interval, whereas disopyramide prolonged it significantly. Importantly, while disopyramide produced serious side effects in 30% of patients, ethmozine was well tolerated with no statistically significant side effects compared with placebo.
Dynamics of right heart flow in patients after Fontan procedure.
Authors: Nakazawa M , Nakanishi T , Okuda H , Satomi G , Nakae S , Imai Y , Takao A
Published: June 2011

In seven patients who underwent Fontan procedures but in whom no valves were inserted, dynamics of right heart flow were evaluated with the use of a catheter-tipped velocity transducer, pulsed Doppler echocardiography, and angiocardiography. Right atrial (RA) contraction caused a forward flow to the pulmonary artery (PA) and a backward flow to the inferior vena cava (IVC). Backward flow to the superior vena cava (SVC) was minimal. As the right atrium relaxed, a rapid forward flow occurred at the IVC and SVC that filled the atrium and a small amount of pulmonary regurgitant flow was observed. Subsequently, a forward flow was observed at the IVC, SVC, and PA during RA diastole. Angiographically determined RA stroke volume (SV) was less than 40% of the left ventricular (LV) SV in three patients in whom the postoperative increase in atrial "a" wave pressure (delta p) was greater than 8 mm Hg, while it was similar to or greater than LVSV in four patients in whom delta p was 6 mm Hg or less. In all patients LV end-diastolic volume was 107 +/- 27(SD)% of normal but LV ejection fraction was 0.53 +/- 0.07, resulting in the reduced cardiac output (2.8 +/- 0.7 l/min/m2). There was no correlation between the RASV or RA ejection fraction and cardiac output. These data show that the RA contraction causes a forward flow to the PA and that pulmonary regurgitation is not significant after Fontan procedure even when valves are not inserted. Also, the postoperative increase in the RA afterload may depress RA function.(ABSTRACT TRUNCATED AT 250 WORDS)
Comparative effects of verapamil, diltiazem, and nifedipine on hemodynamics and left ventricular function during acute myocardial ischemia in dogs.
Authors: Urquhart J , Patterson R E , Bacharach S L , Green M V , Speir E H , Aamodt R , Epstein S E
Published: June 2011

The calcium channel-blocking drugs verapamil, diltiazem, and nifedipine are being used with increasing frequency in patients with angina pectoris due to coronary artery disease. Although each of these agents possesses negative inotropic potential, their relative effects on myocardial function in relation to their vasodilator potencies are unknown. We understood to study this in 20 conscious dogs that had partial occlusions of their circumflex coronary arteries during therapy with placebo, verapamil, nifedipine, or diltiazem. Myocardial blood flow was measured by use of microspheres, and left ventricular function was measured by radionuclide angiography. Drug effects were compared at doses causing equal decreases in mean arterial pressure and coronary vascular resistance of nonischemic myocardium. Global ejection fraction and ejection fraction of the ischemic region were significantly decreased by verapamil (p less than .01) and increased by nifedipine (p less than .001); diltiazem caused no significant changes. Verapamil significantly increased peak diastolic filling rate (p less than .001); nifedipine also increased diastolic filling rate, but only at doses that markedly decreased mean arterial pressure and coronary vascular resistance. The effect of diltiazem on diastolic filling rate was not significantly different than placebo. For doses causing an equal decrease in mean arterial pressure, verapamil decreased heart rate (p less than .001), and diltiazem and nifedipine increased heart rate (p less than .001). We conclude that the relative potencies of these three calcium channel blocking agents on left ventricular systolic and diastolic function during myocardial ischemia are different when compared with their relative vasodilator potencies. These differences may have important clinical implications.
Myocardial contrast two-dimensional echocardiography: comparison of contrast disappearance rates in normal and underperfused myocardium.
Authors: Maurer G , Ong K , Haendchen R , Torres M , Tei C , Wood F , Meerbaum S , Shah P , Corday E
Published: June 2011

A computer algorithm was developed and applied to measure brightness decay rates of myocardial contrast opacification observed with two-dimensional echocardiography (2DE). An agitated mixture of diatrizoate meglumine and saline (Renografin-saline) was injected into the left main coronary artery of 17 closed-chest dogs during the control state as well as after placement of an intracoronary plug to induce 85% stenosis in the left anterior descending coronary artery (LAD) in five dogs. In 12 dogs, injections were also performed distally to complete intracoronary balloon occlusion of the LAD. For each injection, up to 35 electrocardiographic-gated, end-diastolic 2DE frames were digitized into an image-processing computer that determined mean pixel brightness of each of 12 myocardial segments per 2DE short-axis cross-section. Time-activity curves for each segment were generated, and contrast decay half-life (t 1/2) was calculated. Mean t 1/2 for control-state injections was found to be 24.1 +/- 7.7 sec, as opposed to 293.8 +/- 164.5 sec after complete coronary occlusion (p less than .001). In the five dogs in which 85% LAD stenosis was induced, prolongation of contrast t 1/2 from 18.3 +/- 8.9 sec during control to 44.3 +/- 21.0 sec (p less than .001) after plug insertion occurred in myocardial segments subserved by the stenosed vessel. No significant change occurred in segments that were not supplied by the stenosed vessel (21.9 +/- 9.1 sec during control vs 24.9 +/- 11.6 after plug insertion into the LAD). A reproducibility study of injection-to-injection t 1/2 in the control state indicated a correlation coefficient of r = .84 and a standard error of the estimate (SEE) equal to 5.86 sec, while interobserver t 1/2 reproducibility was r = .91 and SEE = 5.21 sec. The t 1/2 measurement derived by computer analysis of myocardial contrast 2DE may serve as an index for characterization of regional myocardial blood flow and may be applicable to evaluate interventions that alter perfusion.
Selective impairment of baroreflex-mediated vasoconstrictor responses in patients with ventricular dysfunction.
Authors: Ferguson D W , Abboud F M , Mark A L
Published: June 2011

Cardiac dysfunction in animals has been associated with impairment of arterial and cardiopulmonary baroreflex control of the circulation. Chronic heart failure in human beings is associated with neurohumoral excitation, which could result in part from impairment in the inhibitory influence of baroreflexes. We postulated that (1) patients with left ventricular dysfunction (LVD) have impaired baroreflex modulation of vascular resistance and (2) administration of a digitalis glycoside would immediately restore baroreflex sensitivity. Eleven patients with LVD (NYHA class, 2.8 +/- 0.2, mean +/- SEM; baseline left ventricular ejection fraction, 18 +/- 2%; cardiac index, 2.4 +/- 0.21/min/m2; and pulmonary capillary wedge pressure, 26.0 +/- 3.2 mm Hg) were compared with 17 normal control subjects. We measured forearm vasoconstrictor responses to simulated orthostatic stress with use of lower body negative pressure (LBNP) at -10 and -40 mm Hg to unload cardiopulmonary and arterial baroreceptors. Baseline forearm vascular resistance (FVR) was higher in patients with LVD than in normal subjects: FVRLVD, 68.8 +/- 15.3 U; FVRN, 23.2 +/- 2.1 U (p less than .001). During unloading of baroreceptors with LBNP -10 mm Hg, normal subjects developed vasoconstriction (delta VRN at LBNP -10 mm Hg, +5.7 +/- 1.6 U) but patients with LVD failed to have vasoconstriction and tended to develop vasodilation (delta FVRLVD at LBNP -10 mm Hg, -8.6 +/- 8.5 U) (p = .05, normals vs patients with LVD at LBNP -10 mm Hg). A more marked disparity in response was seen during unloading of baroreceptors of LBNP -40 mm Hg: delta FVRN at LBNP -40 mm Hg, +16.6 +/- 1.5 U; delta FVRLVD at LBNP -40 mm Hg, -10.3 +/- 9.6 U (p less than .001, normals vs patients with LVD). Despite high baseline values for FVR, patients with LVD developed vasoconstriction during intra-arterial infusions of norepinephrine, thereby excluding a nonspecific depression of vascular reactivity as the mechanism for abnormal responses to LBNP in patients with LVD. We also studied the short-term effects of administration of a digitalis glycoside, ouabain 0.0075 mg/kg (seven patients) or lanatoside C (Cedilanid-D) 0.02 mg/kg (three patients), on baroreflex-mediated vasoconstrictor responses to LBNP in the patients with LVD. Digitalis glycoside reduced baseline FVR from 71.8 +/- 16.6 to 48.6 +/- 12.0 U (p less than .02). Responses to LBNP tended to be normalized after administration of digitalis glycoside: delta FVR during LBNP -40 mm Hg, -11.1 +/- 10.5 U before and +7.8 +/- 5.6 U after the drug (p less than .05).(ABSTRACT TRUNCATED AT 400 WORDS)
The clinical features of isolated left circumflex coronary artery disease.
Authors: Dunn R F , Newman H N , Bernstein L , Harris P J , Roubin G S , Morris J , Kelly D T
Published: June 2011

The clinical characteristics of 84 patients with isolated circumflex disease (greater than or equal to 70% luminal stenosis) were reviewed. A total of 66 patients had angina pectoris (mean duration 17.3 months), and 60 had suffered a myocardial infarction. Risk factors averaged 2.2 per patient. In the 84 patients there were 103 discrete circumflex stenoses; 51 stenoses were central (proximal circumflex, obtuse marginal, and intermediate branches), and 52 were peripheral (distal circumflex, posterolateral, and posterior descending branches); 48 were total and 55 were subtotal. Left ventricular function was normal in 21 patients and abnormal in 63 patients, but the mean left ventricular ejection fraction of the group was normal (59 +/- 12%). Eighty-two patients had abnormal electrocardiograms: there were Q waves in 25, RV pattern in 43, ST-T wave abnormalities in 19, left bundle branch block in two, and pacemaker rhythm in one. Inferior abnormalities on the electrocardiogram correlated with peripheral stenoses (p less than .02), and lateral abnormalities on the electrocardiogram correlated with central stenoses (p less than .01). The RV pattern of true posterior infarction was seen in both central and peripheral stenoses. In the 32 patients who underwent thallium scanning, lateral defects were more common with central stenoses, but posterolateral defects occurred similarly in central and peripheral stenoses. Prognosis was good. There were two deaths during the mean follow-up time of 17 months (range 1 to 49). The cumulative survival rate was 100% at 12 months, 97.5 +/- 2.9% at 24 months, and 97.5 +/- 3.6% at 30 months.
The incidence and natural history of pericardial effusion after cardiac surgery--an echocardiographic study.
Authors: Weitzman L B , Tinker W P , Kronzon I , Cohen M L , Glassman E , Spencer F C
Published: June 2011

One hundred twenty-two consecutive patients (104 men; 18 women) were studied to determine the incidence and natural history of pericardial effusion occurring 2, 5, 10, and 20 to 50 days after cardiac surgery. Three patients had pericardial effusions before and 103 patients (91 men; three women) had effusions after surgery. Effusions were first recorded on the second postoperative day in 72 patients, on the fifth postoperative day in 29 patients, and on the tenth postoperative day in two patients. In 96 of these patients, effusions reached their maximum size by postoperative day 10. Of the 103 patients with effusions, 66 (64%) were followed to complete resolution. A specific pattern was observed in most resolving effusions. The echo-free space diagnostic of pericardial effusion became progressively more echo-dense as the effusion diminished in size. As the effusion became echo-dense, the posterior pericardium, which had been motionless, resumed its normal systolic anterior motion. One patient developed cardiac tamponade on postoperative day 3. We conclude that pericardial effusion occurs frequently after cardiac surgery, but that associated complications are rare.
Role of triple extrastimuli during electrophysiologic study of patients with documented sustained ventricular tachyarrhythmias.
Authors: Buxton A E , Waxman H L , Marchlinski F E , Untereker W J , Waspe L E , Josephson M E
Published: June 2011

Electrophysiologic studies were performed in 172 consecutive patients for evaluation of documented sustained ventricular tachyarrhythmias. One hundred thirteen patients presented with sustained ventricular tachycardia that was hemodynamically stable, and 59 patients presented with cardiac arrest. Seventy-one patients without previously documented or suspected ventricular arrhythmias were also studied to determine the specificity of our electrophysiologic study protocol. The stimulation protocol included single, double, and triple right ventricular extrastimuli and rapid ventricular pacing at multiple cycle lengths performed at one or more right ventricular sites. Stimulation was performed at one or more left ventricular sites in patients with documented spontaneous arrhythmias when right ventricular programmed stimulation failed to induce sustained ventricular tachycardia. Ventricular tachyarrhythmias were induced in 110 (97%) of the patients who presented with sustained ventricular tachycardia, in 48 (81%) of the patients who presented with cardiac arrest, and in 28 (40%) of the patients without documented spontaneous arrhythmias. Right ventricular triple extrastimuli induced tachycardia in 22% of patients who presented with sustained ventricular tachycardia vs 46% of those who presented with cardiac arrest (p less than .001). Left ventricular stimulation was required for tachycardia induction in 3% of patients with stable tachycardia vs 19% of those with cardiac arrest (p less than .01). Triple extrastimuli induced 57% of tachycardias in the 28 patients without spontaneous arrhythmias, and virtually all of these tachycardias were polymorphic and nonsustained. The cycle lengths of tachycardias induced in each group by double and triple extrastimuli were similar, but the tachycardias induced in patients with cardiac arrest were significantly faster than those induced in the ventricular tachycardia group (mean cycle length 218 vs 291 msec, p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
Coronary thrombolysis with intravenously administered human tissue-type plasminogen activator produced by recombinant DNA technology.
Authors: Van de Werf F , Bergmann S R , Fox K A , de Geest H , Hoyng C F , Sobel B E , Collen D
Published: June 2011

Coronary thrombolysis was induced by intravenous infusion of human tissue-type plasminogen activator (recombinant human t-PA or rt-PA) obtained by expression of the cloned gene in a mammalian cell system. Thrombolysis was detected by the appearance of reperfusion arrhythmia and confirmed by repeat angiography in anesthetized dogs with 1-hr-old thrombi of the left anterior descending coronary artery that were induced with a copper coil. Infusion of 1000 IU (10 micrograms)/kg/min intravenous rt-PA (n = 9) elicited reperfusion within 13.7 +/- 1.9 min (mean +/- SE) without producing systemic fibrinolysis or distal coronary embolization. Infusion of urokinase at the same rate elicited thrombolysis in seven of 10 dogs within an average of 19.3 +/- 2.2 min. However, distal coronary embolization occurred in two dogs and systemic fibrinolysis was observed in all. In three dogs treated with urokinase thrombolysis was obtained only with subsequent intracoronary infusion. Restoration of myocardial perfusion and metabolism assessed with positron-emission tomography was consistently noted in dogs treated with rt-PA. Thus, rt-PA, a clot-selective thrombolytic agent that does not activate the fibrinolytic system systemically and that is potentially available in large quantities, in view of its synthesis by recombinant DNA technology, offers a promising practical approach for coronary thrombolysis in patients with acute myocardial infarction.
The inotropic effects of strophanthidin in Purkinje fibers and the sodium pump.
Authors: Bernabei R , Vassalle M
Published: June 2011

The role of the inhibition of the Na pump in strophanthidin inotropy was studied in canine Purkinje fibers by correlating changes in contractile force with changes in maximum diastolic potential caused by conditions that enhance the electrogenic extrusion of Na. It was found that a brief exposure to a zero-K or to a zero-K, zero-Ca solution (but not to a zero-Ca solution) is followed by an increase in maximum diastolic potential. This hyperpolarization is reduced if NaCl is substituted by LiCl and in the presence of tetrodotoxin. In quiescent fibers exposed to tetrodotoxin, the hyperpolarization is abolished. A low concentration of strophanthidin (5 X 10(-8)M) increases contractile force but does not modify the hyperpolarization. Larger strophanthidin concentrations (5 X 10(-7)M to 10(-6)M) increase and then decrease contractile force and reduce or abolish the hyperpolarization. Metabolic inhibitors also reduce the hyperpolarization. We conclude that the positive inotropic effect of a low (therapeutic) concentration of strophanthidin is due to a mechanism other than Na pump inhibition.
Quantitative assessment of growth and function of the cardiac chambers in the normal human fetus: a prospective longitudinal echocardiographic study.
Authors: St John Sutton M G , Gewitz M H , Shah B , Cohen A , Reichek N , Gabbe S , Huff D S
Published: June 2011

We assessed the changes in cardiac chamber size, architecture and function in the normal fetus in a prospective, longitudinal, two-dimensional, and two-dimensionally directed M mode echocardiographic study. Serial echocardiograms were recorded in 16 normal fetuses at 4 week intervals from 20 weeks gestation to parturition. Fetal gestational age was assessed by biparietal diameter. Left ventricular, right ventricular, and left atrial chamber sizes and aortic diameter all increased linearly with age. The ratios of right and left ventricular diameter, left atrial to aortic diameters, and relative left ventricular wall thickness that we used as an index of short-axis left ventricular architecture remained constant. Fractional right ventricular and left ventricular wall thicknesses were similar both on echocardiograms and in postmortem hearts over the same range of gestational ages. In addition, postmortem right ventricular and left ventricular free wall weights were indistinguishable and contributed the same proportion to total heart weight throughout gestation. Left ventricular echocardiographic mass increased linearly from a mean of 0.86 +/- 0.09 to 7.47 +/- 2.43 g at term and corresponded closely with postmortem left ventricular weight. We conclude that (1) fetal cardiac chamber dimensions, wall thicknesses, and left ventricular mass increased with gestational age, (2) cardiac architecture in terms of the ratios of right ventricular/left ventricular diameters, left atrial/aortic diameters, and relative wall thickness remained constant, (3) right and left ventricular fractional shortening did not change with age, (4) left ventricular mass assessed echocardiographically corresponded closely with postmortem left ventricular weights in fetal hearts of similar gestational ages, and (5) the similarities between right and left ventricular sizes, wall thicknesses, and free wall weights in this study do not support the theory of right ventricular dominance in the human fetus.
Vascular structure in lung tissue obtained at biopsy correlated with pulmonary hemodynamic findings after repair of congenital heart defects.
Authors: Rabinovitch M , Keane J F , Norwood W I , Castaneda A R , Reid L
Published: June 2011

At the time of surgical repair, a lung biopsy was performed on patients with congenital heart defects who either had pulmonary hypertension or in whom it would be likely to develop if the lesion were not corrected. Pulmonary vascular changes, assessed morphometrically and also according to the classification of Heath and Edwards (Circulation 18: 533, 1958), were correlated with the postoperative pulmonary hemodynamic findings: mean pulmonary arterial pressure the day after correction and mean pulmonary arterial pressure and pulmonary vascular resistance measured 1 year later. On the first postoperative day, increased mean pulmonary arterial pressure was uncommon in patients with morphometric grade A or B (mild) biopsy findings and Heath-Edwards grade N (normal), and if it was present it was of a mild degree. Mean pulmonary arterial pressure was commonly elevated in those with grade B (severe) or C (mild or severe) and Heath-Edwards grade I biopsy results and was more frequently elevated in those with grade II findings. Moderate-to-severe elevation of mean pulmonary arterial pressure was invariable in patients with Heath-Edwards grade III changes regardless of the morphometric grade. One year after repair, mean pulmonary arterial pressure and/or pulmonary vascular resistance were normal in all patients whose conditions were corrected surgically before 9 months of age regardless of the severity of the pulmonary vascular changes. Values were normal in patients whose conditions were repaired surgically at 9 months of age or later who had grade A or B (mild) morphometric findings with any Heath-Edwards grade or grade B (severe) morphometric findings with Heath-Edwards grade I but were increased in half of the patients with grade B (severe) morphometric findings and Heath-Edwards grade II or with grade C (mild or severe) and Heath-Edwards grade I or II changes. Pulmonary arterial pressure and pulmonary vascular resistance were increased in all patients whose conditions were repaired after 2 years of age with grade C morphometric findings and to a severe degree if associated with Heath-Edwards grade III. Thus, although the Heath-Edwards grade can usually be used to identify patients at risk for pulmonary hypertension in the early postoperative period, both the morphometric and the Heath-Edwards grades as well as the age of the patient at the time of repair can be used to determine whether pulmonary arterial pressure and resistance eventually return to normal or remain elevated.
Effect of heparin on plasma fibrinopeptide A in patients with acute myocardial infarction.
Authors: Mombelli G , Im Hof V , Haeberli A , Straub P W
Published: June 2011

The plasma level of fibrinopeptide A (fpA) was used as an index of thrombin action on fibrinogen in order to investigate the rates of fibrin formation and the effect of heparin on thrombin in patients with acute myocardial infarction. The fpA levels measured on admission in 19 patients with acute myocardial infarction ranged from 1.7 to 12.4 ng/ml and were elevated (greater than 2.5 ng/ml) in 16 patients. A loading dose of 5000 IU of heparin resulted in a significant decrease within 20 min of the mean fpA level (from 5.1 to 2.2 ng/ml; p less than .001) and in an fpA normalization in five of 16 patients. During the following continuous infusion of 20,000 IU of heparin per day, the mean fpA levels measured on day 0, 1, and 2 were 3.0, 3.2, and 3.4 ng/ml, respectively, with 16 of 46 fpA values within the normal range. In 10 additional patients, the effect of higher concentrations of heparin and the consequences of stopping heparin infusion were studied. An additional 5000 IU of heparin injected intravenously during continuous infusion of 20,000 IU of heparin per day resulted in a substantial decrease of the plasma fpA level in three of 10 measurements. The stopping of heparin infusion led to an impressive increase of the mean fpA level (from 3.1 to 12.9 ng/ml; p less than .001) within 2 hr. These data demonstrate increased fibrin formation in patients with acute myocardial infarction and neutralization of thrombin in vivo by heparin.(ABSTRACT TRUNCATED AT 250 WORDS)
Fast-Fourier transform analysis of signal-averaged electrocardiograms for identification of patients prone to sustained ventricular tachycardia.
Authors: Cain M E , Ambos H D , Witkowski F X , Sobel B E
Published: June 2011

Electrocardiograms obtained from patients during arrhythmia-free intervals do not identify those prone to sustained ventricular tachycardia (VT) despite the occult delayed activation that is presumably present. To determine whether frequency-domain analysis facilitates detection of this hallmark of predisposition to VT, fast-Fourier transform analysis (FFTA) procedures were developed and tested with a computer-generated mathematical model. The FFTA approach developed allows inherent limitations of high-gain amplification and a priori filtering used commonly for time-domain analysis to be avoided. After demonstrating that FFTA detected low-amplitude oscillatory waveforms in signal-averaged recordings in the frequency domain, the procedure was applied to signal-averaged X, Y, and Z lead recordings from the following three groups of patients: group I, patients with prior myocardial infarction and episodic sustained VT (n = 16); group II, patients with prior myocardial infarction without overt sustained VT (n = 35); and group III, normal control subjects (n = 10). Results of FFTA demonstrated significant (p less than .0001) differences in the decibel drop at 40 Hz and the area under the curve from the fundamental frequency to the frequency at which the spectral amplitude was decreased by 60 dB for both the terminal 40 msec of the QRS and ST segment in patients in group I compared with those in groups II and III, in whom results were similar. Results were independent of QRS duration (r = .2), left ventricular ejection fraction (r = .19), and complexity of spontaneous ventricular ectopy. Thus, patients known to manifest sustained VT also exhibited relatively greater high-frequency content in arrhythmia-free intervals in the terminal QRS and ST segment than those without VT (88%, 15%, and 0% in groups I through III, respectively). FFTA offers promise for the noninvasive detection of patients at risk for the development of sustained VT.
Coumadin and aspirin in prevention of recurrence after transluminal coronary angioplasty: a randomized study.
Authors: Thornton M A , Gruentzig A R , Hollman J , King S B , Douglas J S
Published: June 2011

To determine the influence of adjunctive treatment with coumadin or aspirin on recurrence rate after percutaneous transluminal coronary angioplasty (PTCA), 248 patients in whom PTCA was assessed to be a primary success were randomized to either 325 mm aspirin daily or to coumadin treatment sufficient to maintain a prothrombin time 2 to 2.5 times the control value. The follow-up protocol included stress testing and coronary angiographic examinations 3 to 6 months after PTCA. All patients were followed for at least 9 months. Of the 122 patients randomized to coumadin 44 (36%) had recurrent stenoses as opposed to 34/126 (27%) of patients on aspirin, a difference that did not reach statistical significance at the .05 level. However, patients with at least a 6 month history of angina demonstrated a significantly different response to adjunctive treatment in that 19/43 (44%) of coumadin patients as compared with 10/48 (21%) of aspirin patients had recurrent stenoses (p less than .05). Thus, coumadin was not shown to be more effective than aspirin as adjunctive treatment after PTCA, while aspirin was shown to be superior to coumadin in patients with a longer history of angina.
Nifedipine therapy for patients with threatened and acute myocardial infarction: a randomized, double-blind, placebo-controlled comparison.
Authors: Muller J E , Morrison J , Stone P H , Rude R E , Rosner B , Roberts R , Pearle D L , Turi Z G , Schneider J F , Serfas D H
Published: June 2011

Preliminary clinical and laboratory observations suggest that nifedipine might prevent progression of threatened myocardial infarction by reversing coronary spasm or might limit necrosis during the course of acute myocardial infarction. We screened 3143 patients with ischemic pain of greater than 45 min duration and randomly assigned 105 eligible patients with threatened myocardial infarction and 66 with acute myocardial infarction to receive nifedipine (20 mg orally every 4 hr for 14 days) or placebo plus standard care. Treatment was started 4.6 +/- 0.1 hr after the onset of pain. Infarct size index was calculated by the MB-creatine kinase (CK) method and expressed as CK-geq/m2 +/- SE. The incidence of progression to infarction among patients with threatened myocardial infarction was not significantly altered by nifedipine (36 of 48 [75%] for placebo-treated and 43 of 57 [75%] for nifedipine-treated patients). Furthermore, infarct size index was similar among placebo- and nifedipine-treated patients (16.9 +/- 1.5 MB-CK-geq/m2, n = 65, and 17.0 +/- 1.5 MB-CK-geq/m2, n = 68, respectively) with threatened myocardial infarction who exhibited infarction and for those with acute myocardial infarction. Among the 171 eligible patients randomly assigned to drug or placebo, 6 month mortality did not differ significantly (8.5% for placebo vs 10.1% for nifedipine, NS), but mortality in the 2 weeks after randomization was significantly higher for nifedipine-treated patients (0% for placebo compared with 7.9% for nifedipine, p = .018).(ABSTRACT TRUNCATED AT 250 WORDS)
Intracoronary thrombolysis in patients with acute myocardial infarction: comparison of the efficacy of urokinase with streptokinase.
Authors: Tennant S N , Dixon J , Venable T C , Page H L , Roach A , Kaiser A B , Frederiksen R , Tacogue L , Kaplan P , Babu N S
Published: June 2011

The efficacy of intracoronary urokinase and streptokinase were compared in 80 patients with acute myocardial infarction in a prospective, randomized, double-blind study. Urokinase was infused into the occluded coronary artery at 6000 U/min, and streptokinase was infused at 2000 U/min. Maximal duration of infusion was 2 hr. The frequency of successfully opening the artery was similar for patients receiving urokinase (27 of 45, 60%) and those receiving streptokinase (20 of 35, 57%). Fibrinogen levels after infusion were measured in 63 patients. Nineteen of 29 streptokinase recipients had fibrinogen levels less than 100 mg/dl compared with levels of two of 34 urokinase recipients (p less than .001). Five of 45 (11%) patients receiving urokinase and 10 of 35 receiving streptokinase (29%) had bleeding complications (p less than .05). Major bleeding after early coronary artery bypass surgery was more frequent in the streptokinase group (four of five compared with a similar group of patients receiving urokinase (none of five). This study demonstrates that while urokinase and streptokinase have equal intracoronary thrombolytic efficacy, patients receiving urokinase have less systemic fibrinolysis and less perioperative bleeding with early surgery than do patients receiving streptokinase.
Measurement of cardioversion/defibrillation thresholds in man by a truncated exponential waveform and an apical patch-superior vena caval spring electrode configuration.
Authors: Winkle R A , Stinson E B , Bach S M , Echt D S , Oyer P , Armstrong K
Published: June 2011

Defibrillation/cardioversion thresholds were measured in 33 patients undergoing defibrillator implants. Each patient had a 12 cm2 patch placed near the left ventricular apex via a thoracotomy and a 10 cm2 spring lead placed pervenously at the right atrial-superior vena caval junction. Ventricular tachycardia of stable morphology, polymorphic ventricular tachycardia, or ventricular fibrillation was induced four times in each patient and 1, 5, 10, and 25 J truncated exponential shocks with 60% tilt were given in a random sequence. The conversion rate was constant (77%, 86%, 87%, 85%) with increasing energy for ventricular tachycardia but progressively increased for polymorphic ventricular tachycardia and ventricular fibrillation (8%, 33%, 58%, 92%). The ventricular tachycardia acceleration rates for 1, 5, 10, and 25 J were 23%, 14%, 10%, and 15%. Patients not reliably converted with 25 J may require repositioning of leads or two patches. We conclude that for the spring-patch electrodes, increasing energy from 1 to 25 J improves the conversion rate for polymorphic ventricular tachycardia and ventricular fibrillation; the ventricular tachycardia conversion rate is constant. Acceleration of ventricular tachycardia occurs at all energies. Defibrillator implantation requires extensive intraoperative electrophysiologic testing to ensure safe and reliable termination of ventricular tachycardia and fibrillation.