bluuebunny/crossref_metadata_2025 huggingface dataset:
The prevalence of peripheral arterial disease in a defined population.
Authors: Criqui M H , Fronek A , Barrett-Connor E , Klauber M R , Gabriel S , Goodman D
Published: June 2011

Because patients with peripheral arterial disease (PAD) may be asymptomatic or may present with atypical symptoms or findings, the true population prevalence of PAD is essentially unknown. We used four highly reliable, sophisticated noninvasive tests (segmental blood pressure, flow velocity by Doppler ultrasound, postocclusive reactive hyperemia, and pulse reappearance half-time) to assess the prevalence of large-vessel PAD and small-vessel PAD in an older (average age 66 years) defined population of 613 men and women. A total of 11.7% of the population had large-vessel PAD on noninvasive testing, and nearly half of those with large-vessel PAD also had small-vessel PAD (5.2%). An additional 16.0% of the population had isolated small-vessel PAD. Large-vessel PAD increased dramatically with age and was slightly more common in men and in subjects with hyperlipidemia. Isolated small-vessel PAD, by contrast, was essentially unrelated to sex, hyperlipidemia, or age, although it was somewhat less common before age 60. Intermittent claudication rates in this population were 2.2% in men and 1.7% in women, and abnormalities in femoral or posterior tibial pulse were present in 20.3% of men and 22.1% of women compared with the noninvasively assessed large-vessel PAD rate of 11.7%. Thus assessment of large-vessel PAD prevalence by intermittent claudication dramatically underestimated the true large-vessel PAD prevalence and assessment by peripheral pulse examination dramatically overestimated the true prevalence.
Influence of coronary collateral blood flow on the development of exertional ischemia and Q wave infarction in patients with severe single-vessel disease.
Authors: Freedman S B , Dunn R F , Bernstein L , Morris J , Kelly D T
Published: June 2011

The functional significance of coronary collateral flow from a nonobstructed supply artery was studied in 121 patients with severe (greater than or equal to 80%) single-vessel disease, 64 with and 57 without Q wave infarction. All patients underwent exercise thallium imaging and coronary angiography. On angiography, collateral flow was present in 85% of 74 occluded arteries compared with only 17% of 47 arteries with subtotal obstruction (p less than .001). Collateral flow was not seen in arteries with lesions of less than 90% obstruction. Collateral flow was present in 100% of 29 occluded arteries in patients without Q wave infarction compared with only 76% of 45 occluded arteries with Q wave infarction (p less than .005). Clinical variables did not correlate with collateral flow. Collateral flow did not prevent ischemia on exercise thallium imaging in patients without Q wave infarction: 30 of 33 (91%) with collateral flow had reversible thallium defects compared with 24 of 24 (100%) without collateral flow (p = NS). In patients with Q wave infarction, partially reversible exercise thallium defects (peri-infarctional ischemia) were more common with flow to the area from either subtotal obstruction (73%) or collateral flow (45%) than with no flow from total occlusion (27%; p = .05). In patients with severe single-vessel disease the presence of collateral flow is principally determined by coronary occlusion. Collateral flow may protect from Q wave infarction but does not prevent exercise ischemia on thallium imaging.
Hydraulic estimation of stenotic orifice area: a correction of the Gorlin formula.
Authors: Cannon S R , Richards K L , Crawford M
Published: June 2011

To determine the source of errors in the Gorlin formula for estimating stenotic valvular orifice area, we used a pulsatile flow model that emulated left ventricular and aortic pressures and flow and allowed control of ventricular outflow orifice area. After comparing orifice areas calculated by the Gorlin formula with actual orifice areas, the Gorlin formula constant (k) was found to be highly correlated with the square root of the mean transvalvular gradient (r = .95). A new formula was derived empirically and predicted areas more accurately and with smaller standard errors than the Gorlin formula in the model (r = .98, SEE = 0.11 and r = .87, SEE = 0.28, respectively) in a series of 19 patients with Hancock porcine xenograft valves (r = .89, SEE = 0.07 and r = .60, SEE = 0.12, respectively) and in the original series of patients reported by Gorlin and Gorlin in proposing the Gorlin formula (r = .93, SEE = 0.11 and r = .91, SEE = 0.12, respectively).
The effect of vasodilator therapy on the clinical outcome of patients with primary pulmonary hypertension.
Authors: Rich S , Brundage B H , Levy P S
Published: June 2011

The short- and long-term hemodynamic effects of vasodilators in patients with primary pulmonary hypertension have been studied, but whether they affect survival is unknown. We measured the short-term response to nifedipine and hydralazine in 23 patients with primary pulmonary hypertension and followed their clinical course over 2 years. A favorable drug response, defined as a fall in the pulmonary vascular resistance of 20% or greater, occurred in 18 patients (78%). Half of the patients who exhibited a favorable short-term response were treated with long-term vasodilator therapy. Their clinical course was compared with that of responders who were not treated and with that of the nonresponders. Of the responders who were treated, two improved, four had no change, and three died; of the responders who were not treated, one improved, three had no change, and five died. Using stepwise Cox regression, we evaluated age, sex, functional class on entry, pulmonary arterial pressure, pulmonary vascular resistance, and short-term drug response as predictors of survival and found only functional class and a favorable short-term drug response to be significant predictors (p less than .01); however, there was no difference in survival between the responders who were treated and those who were not. We conclude that the ability to respond to short-term nifedipine or hydralazine therapy predicts longer survival for patients with primary pulmonary hypertension, but placing patients with a favorable short-term response on long-term vasodilator therapy does not affect the overall outcome.
Comparative efficacy of transvenous cardioversion and pacing in patients with sustained ventricular tachycardia: a prospective, randomized, crossover study.
Authors: Saksena S , Chandran P , Shah Y , Boccadamo R , Pantopoulos D , Rothbart S T
Published: June 2011

We performed a prospective, randomized crossover study to evaluate the comparative efficacy of transvenous cardioversion and rapid ventricular pacing for termination of induced ventricular tachycardia in patients with spontaneous ventricular tachycardia and organic heart disease. Sixty-two episodes of ventricular tachycardia were induced in 15 patients, mean age 60 +/- 10 years, during electrophysiologic studies. All patients underwent a preselected electrical therapy protocol in a randomized crossover sequence. Transvenous cardioversion was performed by an incremental protocol of three sequential shocks (0.5, 1.1, and 2.7 J). Six asynchronous sequential bursts of rapid ventricular pacing (10 and 15 paced stimuli at 90%, 75%, and 65% of ventricular tachycardia cycle length) were used. Mean cycle length of ventricular tachycardia for the study population was 391 +/- 85 msec. The morphology of the tachycardia was left bundle branch block in 27, right bundle branch block in 32, and indeterminate in three. Characteristics of ventricular tachycardia terminated by the two techniques were comparable. Rate of success for termination of tachycardia with the two methods was also comparable (transvenous cardioversion 83%, rapid ventricular pacing 80%; p greater than .1) and these responses were concordant in 78%. The modes of termination of ventricular tachycardia were similar. The incidence of acceleration of ventricular tachycardia per episode with these preselected protocols was also comparable (transvenous cardioversion 11%, rapid ventricular pacing 6%; p greater than .2). Transient supraventricular tachyarrhythmias were more frequent after transvenous cardioversion (23%) than after rapid ventricular pacing (3%). Significant patient discomfort occurred only after transvenous cardioversion (incidence of 57%).(ABSTRACT TRUNCATED AT 250 WORDS)
Risk factors for the development of prosthetic valve endocarditis.
Authors: Calderwood S B , Swinski L A , Waternaux C M , Karchmer A W , Buckley M J
Published: June 2011

Risk factors for the development of prosthetic valve endocarditis (PVE) were analyzed in 2642 patients undergoing initial valve replacement at the Massachusetts General Hospital from 1975 to 1982. Follow-up was available for 2608 patients (98.7%); the mean length of follow-up was 39.8 months. PVE developed in 116 patients (4.4%). The actuarial risk of PVE was 3.1% at 12 months and 5.7% at 60 months. A Cox model was used to identify risk factors for PVE. Recipients of multiple valves had a higher risk of PVE than single valves (p = .01). There was no difference in the risk of PVE for patients receiving aortic valves vs those receiving mitral valves. Recipients of mechanical valves had a higher risk of PVE than recipients of porcine valves in the first 3 months after surgery (p = .02), but the risk of PVE was higher for porcine valve recipients 12 months or more after surgery (p = .004). Despite this difference in the time course of development of PVE, there was no significant difference in the cumulative risk of PVE by 5 years of follow-up between mechanical and porcine valve recipients. Male sex was a risk factor for PVE within 12 months of aortic valve replacement (p = .008) but not thereafter; sex did not influence the risk of PVE after mitral valve replacement. Older patients had a higher risk of late PVE after multiple (p = .04) or mitral valve replacement (p = .08), but not after aortic valve replacement.
Dispersion of ventricular repolarization and arrhythmia: study of two consecutive ventricular premature complexes.
Authors: Kuo C S , Atarashi H , Reddy C P , Surawicz B
Published: June 2011

The effect of two consecutive ventricular premature stimuli (S1S2) during atrial pacing on dispersion of repolarization and inducibility of ventricular arrhythmias was studied in 16 dogs under control conditions and in four dogs in the presence of an increased dispersion of repolarization during atrial pacing induced by general hypothermia and regional warm blood perfusion via selective cannulation of the distal branch of left anterior decending coronary artery. Dispersion of repolarization was measured as the maximal difference between the ends of six simultaneously recorded monophasic action potentials (MAPs) from anterior ventricular surface, and consisted of MAP duration difference and activation time difference. Dispersion of repolarization during atrial pacing at control was 29 +/- 7 msec (activation time difference 4 +/- 6 msec, MAP duration difference 25 +/- 8 msec), that after S1 at paraseptal the site was 81 +/- 8 msec (activation time difference 73 +/- 12 msec, MAP duration difference 8 +/- 5 msec), and that after S1S2 was 148 +/- 27 msec (activation time difference 103 +/- 21, MAP duration difference 44 +/- 26 msec). Neither S1 nor S1S2 induced ventricular arrhythmia. Hypothermia and regional warm blood reperfusion increased dispersion of repolarization during atrial pacing to 70 +/- 22 msec (activation time difference 9 +/- 3 msec, MAP duration difference 61 +/- 19 msec). During hypothermia and regional warm blood reperfusion, S1 produced a dispersion of repolarization of 149 +/- 29 msec (activation time difference 85 +/- 8 msec, MAP duration difference 64 +/- 23 msec) and did not induce ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
Influence of intimal dissection on restenosis after successful coronary angioplasty.
Authors: Leimgruber P P , Roubin G S , Anderson H V , Bredlau C E , Whitworth H B , Douglas J S , King S B , Greuntzig A R
Published: June 2011

We studied 986 patients who underwent follow-up angiography after successful percutaneous transluminal coronary angioplasty (PTCA) to determine the influence of uncomplicated intimal dissection on restenosis rate. Angiographic evidence of intimal dissection after PTCA was present in 248 patients or 25%. After a mean follow-up time of 7 +/- 5 months (SD) the restenosis rate in patients without intimal dissection was 30% compared with 24% in patients with intimal dissection (p = .08). Patients with available transstenotic pressure gradients were divided according to the hemodynamic result into two subgroups: those with final gradients at the conclusion of PTCA of 15 mm Hg or less (n = 638) and those with gradients greater than 15 mm Hg (n = 244). Patients with intimal dissection had a significantly lower restenosis rate than patients without intimal dissection if the final gradient was 15 mm Hg or less (19% vs 28%; p less than .05). If the final gradient was greater than 15 mm Hg, the presence or absence of intimal dissection had no significant influence on restenosis rate, which was 35% and 39%, respectively (p = NS). We conclude that an uncomplicated intimal dissection after a successful coronary angioplasty has no adverse influence on angiographic restenosis. An excellent angiographic long-term outcome can be expected if the intimal dissection is associated with a favorable hemodynamic result.
Electrophysiologic and antiarrhythmic effects of sotalol in patients with life-threatening ventricular tachyarrhythmias.
Authors: Nademanee K , Feld G , Hendrickson J , Singh P N , Singh B N
Published: June 2011

Sotalol is a unique beta-blocker that lengthens cardiac repolarization and effective refractory period (ERP). Its efficacy after intravenous (1.5 mg/kg) and oral (160 to 480 mg bid) administration was therefore evaluated in 37 patients with refractory recurrent ventricular tachycardia/fibrillation (VT/VF). Thirty-five patients, 33 with inducible VT/VF, underwent electrophysiologic testing. Intravenous sotalol lengthened the ERP in the atrium (+24.6%, p less than .01), atrioventricular node (+24.9%, p less than .01), and ventricle (+14.9%, p less than .01). It also significantly lengthened sinus node recovery time, corrected QT interval (QTc), and the AH interval, but not the HV interval. Sotalol prevented reinduction of VT/VF in 15 patients (45.5%). Twenty-five of the 33 patients (15 with positive results of electrophysiologic tests; 10 with negative results) were given oral sotalol. The drug was ineffective in seven (26.9%) and aggravated arrhythmia in one (3.8%). In four patients sotalol was withdrawn because of side effects; arrhythmias recurred late in two (7.7%). Eleven patients (42.3%) have continued on oral sotalol over a mean follow-up period of 9.2 +/- 8.6 months. Sotalol reduced (n = 21) total premature ventricular complex (PVC) count on the Holter electrocardiogram by 73% (p less than .01), paired PVCs by 89% (p less than .01), and beats of ventricular tachycardia by 95% (p less than .01). In 52% (n = 11), total reduction in PVCs was at least 85%, and incidence of paired and tachycardiac beats was reduced at least 90% (group A). In the remainder (n = 10), PVC suppression was not significant (group B). Group A included nine patients with nonreinducible VT/VF and two in whom it was reinducible; in group B, eight of 10 patients had reinducible VT/VF. The difference between the two groups (Fisher exact test) was significant (p less than .01). The prevention of reinduction of VT/VF by intravenous sotalol and suppression of spontaneously occurring arrhythmias by the oral drug were both predictive of long-term drug efficacy. Sotalol is a significant advance in the short- and long-term management of life-threatening ventricular tachyarrhythmias.
Angle dependence of ultrasonic backscatter in arterial tissues: a study in vitro.
Authors: Picano E , Landini L , Distante A , Salvadori M , Lattanzi F , Masini M , L'Abbate A
Published: June 2011

The object of this study was to obtain quantitative data on the angle dependence of reflected ultrasound signals in freshly excised normal human arterial walls and those with different degrees of atherosclerotic involvement (fatty, fibrofatty, fibrous, or calcified). Fifteen specimens were evaluated in each pathologic subset. The backscatter coefficient (BS, expressed as cm-1 X steradians -1), measured at the single frequency of 10 MHz, was evaluated at a normal angle of incidence of the interrogating beam to the tissue sample and over an angular span of 60 degrees (+/- 30 degrees around normal incidence, 2 degree steps). BS measured at normal incidence separated normal (10(-2) X 0.155 +/- 0.018; mean +/- SE) from fibrofatty (10(-1) X 0.0103 +/- 0.008), fibrous (10(-1) X 0.182 +/- 0.016), and calcified (0.202 +/- 0.016) specimens; normal and fatty (10(-3) X 0.759 +/- 0.142) and fibrofatty and fibrous samples could not be distinguished from each other in a statistically significant way. Angular scattering measurements identified two patterns: A "directive" pattern, characterized by a strongly angle-dependent BS that falls abruptly when the beam is moved slightly away from normal incidence. This pattern was typical of calcified, fibrous, and less markedly, fibrofatty and normal samples. A "nondirective" pattern, characterized by a BS that is not significantly angle dependent and fluctuates throughout the entire angular range. This was typical of fatty samples.
Fetal atrioventricular valve insufficiency associated with nonimmune hydrops: a two-dimensional echocardiographic and pulsed Doppler ultrasound study.
Authors: Silverman N H , Kleinman C S , Rudolph A M , Copel J A , Weinstein E M , Enderlein M A , Golbus M
Published: June 2011

Of 466 fetuses who underwent cardiac ultrasound examination with cross-sectional and M mode echocardiography and pulsed Doppler ultrasound and in whom we were able to follow the natural history, 12 were found to have atrioventricular valve insufficiency and nonimmune hydrops. Eleven fetuses (all of whom had structural heart disease) died either in utero or during the early postnatal period. In the one surviving hydropic fetus with supraventricular tachyarrhythmia and atrioventricular valve regurgitation but without structural heart disease, all the abnormalities disappeared on treatment with digoxin and verapamil. Seven fetuses who had atrioventricular valve insufficiency but did not develop nonimmune hydrops all survived pregnancy and the early neonatal period. The syndrome of atrioventricular valve insufficiency, nonimmune hydrops, and structural heart disease has a poor prognosis. The hydrops in this instance reflects fetal cardiac failure related to venous hypertension and low colloid oncotic pressure.
Left ventricular pulsus alternans in patients with hypertrophic cardiomyopathy and severe obstruction to left ventricular outflow.
Authors: Cannon R O , Schenke W H , Bonow R O , Leon M B , Rosing D R
Published: June 2011

Left ventricular pulsus alternans (LVPA), a rhythmic beat to beat variation in left ventricular systolic pressure and outflow gradient, was noted in 35 of 200 ventricular systolic pressure and outflow gradient, was noted in 35 of 200 patients with hypertrophic cardiomyopathy undergoing hemodynamic study. LVPA was not associated with significant systemic pulsus alternans nor right ventricular pulsus alternans. All patients with LVPA had severe outflow gradients at rest or during provocation. Of 61 patients with severe basal outflow gradients (greater than 80 mm Hg), 12 demonstrated LVPA at rest. Eight of these patients underwent ventricular septal myotomy-myectomy; all had successful abolition of basal outflow gradient. Of the seven of these eight patients who underwent postoperative hemodynamic study and who were in sinus rhythm, none demonstrated LVPA. Eleven of 60 patients with basal outflow gradients ranging from 10 to 70 mm Hg demonstrated LVPA during maneuvers provocative for outflow gradients (mean gradient 90 +/- 37 mm Hg). Two of these patients underwent ventricular septal myotomy-myectomy; neither had a gradient nor LVPA during provocation postoperatively. Twelve additional patients with basal outflow gradients ranging from 0 to 115 mm Hg had LVPA after ectopic beats, generally occurring during maneuvers provocative for outflow gradients, associated with severe outflow gradients (mean gradient 130 +/- 39 mm Hg) during the postextrasystolic beat. None of the 41 patients without an outflow gradient, basal or during provocation, was found to have LVPA. Thus LVPA is commonly seen in during provocation, was found to have LVPA. Thus LVPA is commonly seen in patients with hypertrophic cardiomyopathy and severe left ventricular outflow gradients and may represent inadequate left ventricular contractile function in the presence of high left ventricular systolic pressures.
Quantitative angiographic morphology of coronary stenoses leading to myocardial infarction or unstable angina.
Authors: Wilson R F , Holida M D , White C W
Published: June 2011

Identification of a characteristic morphology of a coronary stenosis likely to result in myocardial infarction would facilitate the prospective evaluation of infarct prevention strategies and identification of high-risk patients. We postulated that coronary lesions associated with recent myocardial infarction or unstable angina would have an angiographic morphology suggesting disruption of an atherosclerotic plaque and would appear morphologically different from lesions associated with chronic stable angina. To test this hypothesis, quantitative coronary angiography (Brown-Dodge method) was performed in 15 patients 4 to 30 days after myocardial infarction, in 10 patients with the abrupt onset of unstable angina and single-vessel coronary disease, and in 15 patients with chronic stable angina without prior myocardial infarction. Serial arterial diameters (20 to 40) within each lesion were determined and the degree of luminal irregularity was quantitated by calculation of an "ulceration" index. The majority of all lesions analyzed resulted in severe luminal stenosis (mean 78% area stenosis, all groups). Despite small differences in mean lesion severity among groups, overlap in the degree of luminal compromise prevented precise classification of lesions associated with myocardial infarction or unstable angina based on percent stenosis or minimum luminal cross-sectional area. The mean ulceration index of lesions in patients with unstable angina and in the infarct-related vessel in those with acute myocardial infarction was 0.62 +/- 0.05 (+/- SEM) and 0.61 +/- 0.03, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Vasoconstriction of stenotic coronary arteries during dynamic exercise in patients with classic angina pectoris: reversibility by nitroglycerin.
Authors: Gage J E , Hess O M , Murakami T , Ritter M , Grimm J , Krayenbuehl H P
Published: June 2011

To study the vasomotility of normal and diseased coronary arteries during dynamic exercise, symptom-limited supine bicycle exercise during cardiac catheterization was performed by 18 patients with classic angina pectoris. The cardiovascular response was assessed by hemodynamic measurements and computer-assisted determination of normal and stenotic coronary artery luminal areas from biplane coronary angiograms made before, during, and after exercise. After baseline measurements were recorded, 12 patients (group 1) performed bicycle exercise for 3.4 min (mean), reaching a maximum workload of 81 W (mean); at the end of exercise they received 1.6 mg sublingual nitroglycerin. After measurements at rest in six other patients (group 2), 0.1 mg intracoronary nitroglycerin was given, followed by exercise (3.8 min, 96 W; NS) and sublingual nitroglycerin as in group 1. During exercise in group 1, luminal area of the coronary stenosis decreased to 71% of resting levels (p less than .001), while area of the normal coronary artery increased to 123% of control (p less than .001). After sublingual nitroglycerin at the end of exercise, area of the normal vessel further increased to 140% of control (p less than .001), while luminal area of the stenosis dilated to 112% of resting levels (p less than .001 vs exercise, NS vs rest). Pretreatment with intracoronary nitroglycerin increased both normal (121%; p less than .05) and stenotic (122%; p less than .05) luminal areas, while preventing the previously observed narrowing of stenosis during exercise (114%; NS). Exercise resulted in a similar heart rate-systolic pressure product and caused angina pectoris in two-thirds of the patients in each group. However, patients pretreated with intracoronary nitroglycerin (group 2) had a lower mean pulmonary arterial pressure during maximum exercise (35 mm Hg) than those patients (group 1) not receiving pretreatment (47 mm Hg; p less than .001). Group 2 patients reached a percentage of their predicted work capacity (65%) that was about the same as that during previous upright bicycle exercise (71%; NS), while group 1 patients had a significantly lower work capacity (51% of predicted) than that before catheterization (82%; p less than .001). Hence, narrowing of coronary artery stenosis during dynamic exercise is attributable to active vasoconstriction due to its reversibility by preexercise intracoronary nitroglycerin. Patients who did not experience narrowing of stenosis during exercise (group 2) had less evidence of myocardial ischemia (lower mean pulmonary arterial pressure) and maintained their work capacity.(ABSTRACT TRUNCATED AT 400 WORDS)
Short-term myocardial uptake of lidocaine and mexiletine in patients with ischemic heart disease.
Authors: Horowitz J D , Dynon M K , Woodward E , Sia S T , Macdonald P S , Morgan D J , Goble A J , Louis W J
Published: June 2011

Determination of short-term myocardial drug uptake and subsequent redistribution was performed in 27 patients with ischemic heart disease for the antiarrhythmic agents lidocaine and mexiletine, using frequent simultaneous measurements of drug concentration in aortic and coronary sinus blood, combined with measurement of coronary sinus blood flow after intravenous bolus injection of the drug. Maximal myocardial drug content per unit resting coronary sinus blood flow (MDC:F) was significantly greater in patients in whom coronary sinus pacing at 100 beat/min was performed during the initial period of drug uptake. Maximal myocardial drug content occurred after 2.4 +/- 0.2 (SEM) for lidocaine and after 5.5 +/- 0.6 min for mexiletine (p less than .001), and pacing did not affect time to maximum myocardial drug content. In nonpaced, but not paced, patients maximal MDC:F was greater in the lidocaine group than that in the mexiletine group. The subsequent efflux of lidocaine from the myocardium was more rapid that that of mexiletine in both paced and nonpaced groups.
Ventricular tachycardia in a young population without overt heart disease.
Authors: Deal B J , Miller S M , Scagliotti D , Prechel D , Gallastegui J L , Hariman R J
Published: June 2011

Since 1974, 24 young patients presenting with ventricular tachycardia and without clinical evidence of heart disease were evaluated and followed. Sixteen patients (67%) were symptomatic. Clinical episodes of ventricular tachycardia were sustained in 18, incessant in four, and nonsustained in two patients. The rate of tachycardia ranged from 130 to 300 beats/min (mean = 200 beats/min). Subtle abnormalities of cardiac size or function were present at cardiac catheterization in 16 of 23 patients (70%). During electrophysiologic studies, spontaneous ventricular tachycardia was present in six patients. The clinical ventricular tachycardia was inducible by programmed stimulation in 13 of 18 patients. The site of origin of tachycardia based on endocardial mapping in 17 patients was the right ventricle in 14, the ventricular septum in one, and indeterminate in two patients. Seventeen patients were treated based on results of short-term drug testing. During a mean follow-up period of 7.5 years, three patients died suddenly; none of these patients were receiving antiarrhythmic medication at the time of death. We conclude that in a young population without clinical evidence of heart disease, ventricular tachycardia may be the first manifestation of cardiomyopathy, since at least two-thirds of these patients have abnormalities at cardiac catheterization. Without treatment mortality in this population may be as high as 13% over an 8 year period. Presently we recommend treatment of ventricular tachycardia in any symptomatic patient, with therapy guided by electrophysiologic and treadmill testing. In addition, we recommend treatment for any asymptomatic patient with exercise-related tachycardia, since this group appears to be at increased risk for sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)
Surgery for Wolff-Parkinson-White syndrome: further experience with an epicardial approach.
Authors: Guiraudon G M , Klein G J , Sharma A D , Jones D L , McLellan D G
Published: June 2011

We have previously reported the use of an epicardial approach for ablation of left ventricular free wall accessory atrioventricular pathways. The technique involves mobilization of the atrioventricular fat pad and exposure and cryoablation of the atrioventricular junction at the site of the accessory pathway on the normothermic beating heart. Here we describe our further experience with left ventricular free wall accessory pathways and right ventricular free wall accessory pathways. Our experience is based on 53 consecutive patients. There were 35 male and 18 female subjects, 6 to 52 (mean 41.4) years old. Forty-eight patients had a left ventricular free wall accessory pathway, and five had a right ventricular free wall accessory pathway. Two patients had an associated anterior septal accessory pathway. Five patients had associated cardiac abnormalities, including atrial septal defect, aortic insufficiency, mitral valve prolapse, Ebstein's anomaly, and cardiomyopathy. The accessory pathway was ablated in 52 patients who remain arrhythmia free without medication after a mean follow-up period of 12 months. The accessory pathway was permanently modified in one patient. There were no postoperative complications. This epicardial approach can be performed with normothermic cardiopulmonary bypass or without bypass. It does not require cross-clamping of the aorta, allowing a greater margin of safety when this is required for concomitant procedures.
Does verapamil improve left ventricular relaxation in patients with myocardial hypertrophy?
Authors: Hess O M , Murakami T , Krayenbuehl H P
Published: June 2011

A beneficial effect of verapamil on left ventricular relaxation has been reported in patients with hypertrophic cardiomyopathy. The effect of 0.1 mg/kg intravenous verapamil on left ventricular relaxation and diastolic mechanics was studied in 10 patients with hypertrophic cardiomyopathy and 13 patients with aortic stenosis. M mode echocardiograms and left ventricular high-fidelity pressure measurements were obtained simultaneously in patients at rest and 10 to 15 min after verapamil. The time constant of left ventricular pressure decay (T; in msec) and the pressure intercept (PB; in mm Hg) were calculated from left ventricular pressure and negative dP/dt during isovolumetric relaxation with the use of a linear regression analysis. Left ventricular early and mean diastolic filling rates as well as diastolic pressure-diameter relationships before and after verapamil were determined from simultaneous echocardiographic and pressure measurements. After verapamil heart rate, left ventricular peak systolic pressure, and maximum and minimum dP/dt remained unchanged in both groups. Left ventricular end-diastolic pressure increased significantly from 15 to 17 mm Hg (p less than .02) in patients with aortic stenosis but did not change in those with hypertrophic cardiomyopathy. However, the time constant T decreased significantly from 79 to 60 msec (p less than .001) in patients with hypertrophic cardiomyopathy but increased significantly from 53 to 68 msec (p less than .025) in those with aortic stenosis. Parallel to the decrease in time constant, early (5.3 vs 7.3 cm/sec, p less than .05) and mean (3.0 vs 4.3 cm/sec, p less than .06) diastolic lengthening rate increased in patients with hypertrophic cardiomyopathy after verapamil. In contrast, early (7.7 vs 7.6 cm/sec, p = NS) and mean (4.3 vs 4.2 cm/sec, p = NS) diastolic lengthening rate remained unchanged in patients with aortic stenosis. The diastolic pressure-diameter relationship did not change in either group after verapamil. Cycle efficiency of the left ventricular pressure-diameter loop was significantly decreased in patients with hypertrophic cardiomyopathy when compared with that in those with aortic stenosis (71% vs 80%; p less than .01), but improved significantly from 71% to 77% (p less than .02) in patients with hypertrophic cardiomyopathy and remained unchanged in those with aortic stenosis (80% vs 80%) after verapamil. We conclude that verapamil improves left ventricular relaxation in patients with hypertrophic cardiomyopathy but delays relaxation in those with aortic stenosis.(ABSTRACT TRUNCATED AT 400 WORDS)
Synergism of thrombolytic agents in vivo.
Authors: Collen D , Stassen J M , Stump D C , Verstraete M
Published: June 2011

The existence of significant synergism between tissue-type plasminogen activator (t-PA) and single-chain urokinase-type plasminogen activator (scu-PA), and between t-PA and urokinase in thrombolysis in vivo is described. In a quantitative preparation of thrombolysis, consisting of rabbits in which a blood clot was induced in the jugular vein with 125I-labeled fibrin, intravenous infusion over 4 hr of t-PA, scu-PA, or urokinase in amounts of 0.5, 1.0, or 2.0 mg/kg body weight resulted in significant thrombolysis (30% to 60%). The simultaneous infusion of t-PA and scu-PA or of t-PA and urokinase had a significantly greater (p less than .001) thrombolytic effect than could be anticipated on the basis of the added effects of each agents alone. However, no synergism was observed between scu-PA and urokinase. The observed alpha 2-antiplasmin consumption and fibrinogen breakdown after urokinase at higher doses did not occur with the equivalent thrombolytic combinations of t-PA and urokinase. The combined use of synergic thrombolytic agents in patients may permit a significant reduction in total administered doses, probably with elimination of the systemic activation of the fibrinolytic system and the concomitant fibrinogen breakdown that is unavoidable with the currently used thrombolytic doses of each agent.
Quantification of myocardial infarct size by thallium-201 single-photon emission computed tomography: experimental validation in the dog.
Authors: Prigent F , Maddahi J , Garcia E V , Satoh Y , Van Train K , Berman D S
Published: June 2011

To evaluate the potential advantages of thallium-201 (201T1) single-photon emission computerized tomography (SPECT) to assess myocardial infarct size in the experimental animal, six normal dogs and 14 dogs with 6 to 8 hr closed-chest coronary occlusion (eight left anterior descending and six left circumflex) were studied. Ten minutes after intravenous administration of 2 mCi of 201T1, 30 projections were obtained over 180 degrees. The dogs were killed and their hearts sliced and stained by triphenyl tetrazolium chloride (TTC). Pathologic infarct size was calculated for each slice and for the entire left ventricular myocardium as percent weight. Tomograms were quantified by automatically generating maximum-count circumferential profiles, which were compared with normal limit profiles derived from the six normal dogs. Tomographic infarct size was defined as the percentage of circumferential points falling below normal for each tomogram. SPECT and TTC infarct size on 71 slices correlated highly (mean +/- SD 27.9 +/- 23.4% and 26.7 +/- 25.3%, respectively; r = .93, p less than .001, SEE = 9.4%). To determine SPECT infarct size as percent total left ventricular myocardial weight, infarct sizes from each slice were added to one another after each was multiplied by a coefficient that reflected the contribution of that slice to the total left ventricular weight. SPECT and TTC infarct size for the entire left ventricle correlated closely (mean +/- SD 20.5 +/- 7.6% and 19.3 +/- 8.3%, respectively; r = .86, p less than .001, SEE = 4.5%). It is concluded that 201T1 SPECT is a valid method for the noninvasive assessment of experimental myocardial infarct size.
Rapid ventricular pacing in the dog: pathophysiologic studies of heart failure.
Authors: Armstrong P W , Stopps T P , Ford S E , de Bold A J
Published: June 2011

We examined rapid ventricular cardiac pacing as a means of inducing heart failure in the dog to establish the sequence and nature of physiologic compensation in this preparation. Seven animals paced at 250 beats/min for 3 weeks (VP1 group) showed an increase in cardiac size from 78.5 +/- 9.5(SD) to 105.8 +/- 13.0 cm2, a reduction in mean arterial pressure from 149 +/- 7 to 130 +/- 21 mm Hg, a fall in cardiac index from 196 +/- 57 to 125 +/- 37 ml/kg/min, and an increase in left ventricular filling pressure from 6 +/- 5 to 22 +/- 9 mm Hg and in right atrial pressure from 2 +/- 2 to 5 +/- 3 mm Hg. An additional series of six animals (VP2 group) was paced until a clear biologic end point for heart failure was reached (average 5.3 +/- 1.9 weeks) and they showed similar but more advanced changes compared with the VP1 group. The changes in cardiac size and hemodynamics in the VP1 and VP2 groups were significantly different from those in parallel studies of 10 sham-operated animals. Plasma norepinephrine and renin activity were unchanged in sham-operated animals, whereas in the VP1 group, plasma norepinephrine rose from 338 +/- 118 to 764 +/- 567 pg/ml (p less than .05), but plasma renin activity did not change. In the VP2 group norepinephrine rose from 471 +/- 285 to 999 +/- 425 pg/ml (p less than .025) and plasma renin rose from 2.1 +/- 1.5 to 8.0 +/- 7.1 ng/ml/hr (p less than .05). There was an excellent correlation between plasma norepinephrine and renin activity before the animals were killed in both the VP1 and VP2 groups (r = .88, p less than .001). No change was evident in atrial natriuretic factor content, as determined by bioassay, in sham-operated or VP1 group animals. However, there was a significant reduction in atrial natriuretic activity from the right atrium that was inversely correlated with the level of right atrial pressure in the VP2 group.
Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.
Authors: Murry C E , Jennings R B , Reimer K A
Published: June 2011

We have previously shown that a brief episode of ischemia slows the rate of ATP depletion during subsequent ischemic episodes. Additionally, intermittent reperfusion may be beneficial to the myocardium by washing out catabolites that have accumulated during ischemia. Thus, we proposed that multiple brief ischemic episodes might actually protect the heart from a subsequent sustained ischemic insult. To test this hypothesis, two sets of experiments were performed. In the first set, one group of dogs (n = 7) was preconditioned with four 5 min circumflex occlusions, each separated by 5 min of reperfusion, followed by a sustained 40 min occlusion. The control group (n = 5) received a single 40 min occlusion. In the second study, an identical preconditioning protocol was followed, and animals (n = 9) then received a sustained 3 hr occlusion. Control animals (n = 7) received a single 3 hr occlusion. Animals were allowed 4 days of reperfusion thereafter. Histologic infarct size then was measured and was related to the major baseline predictors of infarct size, including the anatomic area at risk and collateral blood flow. In the 40 min study, preconditioning with ischemia paradoxically limited infarct size to 25% of that seen in the control group (p less than .001). Collateral blood flows were not significantly different in the two groups. In the 3 hr study, there was no difference between infarct size in the preconditioned and control groups. The protective effect of preconditioning in the 40 min study may have been due to reduced ATP depletion and/or to reduced catabolite accumulation during the sustained occlusion. These results suggest that the multiple anginal episodes that often precede myocardial infarction in man may delay cell death after coronary occlusion, and thereby allow for greater salvage of myocardium through reperfusion therapy.
Changes in intracardiac blood flow velocities and right and left ventricular stroke volumes with gestational age in the normal human fetus: a prospective Doppler echocardiographic study.
Authors: Kenny J F , Plappert T , Doubilet P , Saltzman D H , Cartier M , Zollars L , Leatherman G F , St John Sutton M G
Published: June 2011

We used Doppler echocardiography to quantitate the changes in intracardiac blood flow velocities and right and left ventricular stroke volumes in 80 normal human fetuses from 19 to 40 weeks gestation. Blood flow velocity spectra across the aortic, pulmonary, tricuspid, and mitral valves were digitized to obtain peak velocities (m/sec) and flow velocity integrals. Aortic and pulmonary diameters were measured at valve level from two-dimensional echocardiographic images and cross-sectional area was calculated assuming a circular orifice. Ventricular stroke volume was calculated as the product of the cross-sectional area of a great vessel and the flow velocity integral through that vessel. The pulmonary arterial and aortic diameters increased linearly with gestational age (r = .82, r = .84), and pulmonary arterial diameter consistently exceeded aortic diameter. There was a positive relationship between stroke volume and gestational age: stroke volume increased exponentially from 0.7 ml at 20 weeks to 7.6 ml at 40 weeks for the right ventricle (r = .87) and from 0.7 ml at 20 weeks to 5.2 ml at 40 weeks for the left ventricle (r = .91). Similar results were obtained for right and left ventricular and combined cardiac outputs. In 44% of the fetuses it was possible to quantitate both right and left ventricular stroke volumes. There was a close correlation between right and left ventricular stroke volumes in these fetuses (r = .96) and right ventricular stroke volume exceeded left ventricular stroke volume by 28%.(ABSTRACT TRUNCATED AT 250 WORDS)
Calcitonin gene-related peptide: a potent dilator of human epicardial coronary arteries.
Authors: McEwan J , Larkin S , Davies G , Chierchia S , Brown M , Stevenson J , MacIntyre I , Maseri A
Published: June 2011

To investigate the action of calcitonin gene-related peptide (CGRP) on human epicardial coronary arteries, six patients received intracoronary CGRP at doses of 50,100, and 200 ng/min. The effect of CGRP was measured angiographically with a computerized analysis system. A dose-dependent increase in coronary arterial diameter was observed. At the highest dose there were 34%, 7%, 38%, and 40% mean increases in the diameters of the circumflex, proximal, mid, and distal left anterior descending arteries, respectively. No further increase in diameter was found after a subsequent dose of 1 mg intracoronary isosorbide dinitrate. Prior infusion of CGRP did not prevent coronary arterial spasm induced by ergonovine in two patients with variant angina, but a subsequent bolus of CGRP partially relieved the spasm. We propose that CGRP has a role in the regulation of coronary vascular smooth muscle tone.
Central nervous system effects of beta-adrenergic-blocking drugs: the role of ancillary properties.
Authors: Kostis J B , Rosen R C
Published: June 2011

Among the side effects commonly reported with the use of beta-blockers are symptoms related to the central nervous system (CNS). In this study we compared the effects of four beta-blockers with different ancillary properties (atenolol, metoprolol, propranolol, and pindolol) and placebo on objective and subjective measures of CNS function in 30 healthy male subjects. All subjects were randomly assigned to a double-blind, placebo controlled, Latin-square design study in which five 1 week periods of drug or placebo administration were separated by 2 week washout periods. Laboratory evaluations were conducted at the end of each treatment period, and included multistage exercise stress testing; questionnaire assessments of mood state, sexual function, and sleep habits; tests of psychomotor function; and overnight polysomnographic measures of sleep. Significant effects on sleep continuity were observed for each of the lipophilic drugs, as reflected in the number of awakenings (pindolol = 6.4 +/- 5.0; propranolol = 6.3 +/- 3.2; metoprolol = 7.2 +/- 4.7; atenolol = 3.6 +/- 2.9; placebo = 3.9 +/- 2.7) and time of wakefulness (pindolol = 20.6 +/- 27.0 min; propranolol = 15.5 +/- 23.0 min; metoprolol = 19.5 +/- 24.3 min; atenolol = 10.2 +/- 11.6 min; placebo = 9.2 +/- 74.5 min). Only pindolol significantly affected rapid eye movement (REM) sleep time (pindolol = 54.5 +/- 21.9 min; placebo = 74.5 +/- 74.5 min) and REM latency (pindolol = 175.0 +/- 60.7 min; placebo = 95.4 +/- 43.8 min). Subjective reports of sleep similarly indicated increased wakefulness and greater restlessness with lipophilic beta-blockers.(ABSTRACT TRUNCATED AT 250 WORDS)
Pathogenesis of persistent truncus arteriosus and dextroposed aorta in the chick embryo after neural crest ablation.
Authors: Nishibatake M , Kirby M L , Van Mierop L H
Published: June 2011

To investigate the contribution of cranial neural crest cells to the developing cardiovascular system in the chick embryo, cauterization of various regions of cranial neural crest was performed. Five regions may be distinguished, each of which contributes mesenchyme to pharyngeal (branchial) arches 1 through 4 and 6. Ablation of arch 3, 4, and 6 regions resulted in a high incidence of persistent truncus arteriosus (PTA) associated with anomalies of the aortic arch. Dextroposed aorta (DPA) or anomalies of the inflow tract were found in all ablation groups. Although anomalies of the aortic arch arteries were induced in all ablation groups and were usually associated with intracardiac anomalies, those of the third and right fourth aortic arch were most frequent in the arch 4 and arch 4 + 6 groups. Anomalies of the sixth aortic arch were most frequent after extensive ablations that included the arch 6 region. We speculate that PTA is a direct result of the decreased population of mesenchymal cells derived from the arch 3 through 6 neural crest regions. DPA or anomalies of the inflow tract may be related to altered hemodynamics due to anomalies induced by neural crest ablation. Anomalies of the aortic arch arteries may be caused by either the direct or indirect process.
Intramyocardial variability in integrated backscatter: effects of coronary occlusion and reperfusion.
Authors: Sagar K B , Rhyne T L , Warltier D C , Pelc L , Wann L S
Published: June 2011

The present study was undertaken to characterize regional myocardial alterations of reflected ultrasound during the cardiac cycle in normal, ischemic, and postischemic reperfused myocardium. Time-averaged integrated backscatter (IB) and cardiac cycle-dependent amplitude modulation were measured from subepicardial, midmyocardial, and subendocardial regions of the left ventricular apex and the midportion of the right ventricular free wall under normal conditions (n = 5), after 1 hr of 100% acute left anterior descending (LAD) occlusion (n = 8), and after 15 min LAD occlusion plus 120 min reperfusion (n = 5) in anesthetized, ventilated open-chest dogs. A significant increase in time-averaged IB was observed in the subepicardium, the midmyocardium, and the subendocardium during ischemia and reperfusion, but there was no intramyocardial variability. Cardiac cycle-dependent amplitude modulation of IB was significantly higher in the normal subendocardium than in the subepicardium (4.3 +/- 0.6 vs 2.9 +/- 0.8 dB, p less than .01) and midmyocardium (2.8 +/- .05 dB, p less than .01). This transmural gradient in amplitude modulation was abolished during ischemia and reperfusion. We conclude that cardiac cycle-dependent amplitude modulation in IB has a transmural dependence in the normal myocardium and this is abolished during acute myocardial ischemia.