bluuebunny/crossref_metadata_2025 huggingface dataset:
A new method to calculate aortic valve area without left heart catheterization.
Authors: Warth D C , Stewart W J , Block P C , Weyman A E
Published: June 2011

Assessment of the severity of aortic stenosis remains a commonly encountered clinical problem. Noninvasive evaluation has to date not proven sufficiently accurate in most cases to permit clinical decision making in the individual patient. Therefore, cardiac catheterization and measurement of the valve area with use of the Gorlin equation remains the standard approach in patients with suspected aortic stenosis. Doppler ultrasound allows direct measurement of blood velocity in cardiac chambers. This technique was used to study 16 patients with suspected aortic stenosis after cardiac catheterization. Aortic valve area (AVA) was calculated with the equation AVA = CO/(SEP X mean velocity), where CO is cardiac output measured by thermodilution and SEP is the systolic ejection period derived from the Doppler tracings. The resulting value was compared with valve area calculated from cardiac catheterization data and an excellent correlation was noted (r = .99). This study demonstrates that Doppler ultrasound can be used to accurately measure aortic valve area without the need for left heart catheterization.
Morphologic determinants of hemodynamic state after ventricular septal myotomy-myectomy in patients with obstructive hypertrophic cardiomyopathy: M mode and two-dimensional echocardiographic assessment.
Authors: Spirito P , Maron B J , Rosing D R
Published: June 2011

To define the morphologic features of the left ventricle after ventricular septal myotomy-myectomy and to elucidate the structural changes associated with a postoperative reduction in the pressure gradient, 28 patients with obstructive hypertrophic cardiomyopathy were studied with M mode and qualitative and quantitative two-dimensional echocardiography. Nine patients with a marked reduction in the pressure gradient (no or small, less than or equal to 25 mm Hg, residual basal gradient) demonstrated a marked reduction in septal thickness after surgery (23 +/- 6 to 13 +/- 4 mm; p less than .01), a concomitant increase in septal to mitral valve distance (20 +/- 2 to 30 +/- 5 mm; p less than .005), and a loss or substantial decrease in the magnitude of systolic anterior motion of the mitral valve. Two-dimensional echocardiographic results demonstrated an increase of over 100% in the cross-sectional area of the left ventricular outflow tract at onset of systole (2.2 +/- 0.6 to 5.5 +/- 3 cm2; p less than .01). In six of the patients postoperative paradoxic septal motion appeared to contribute importantly to the increased size of the outflow tract during ventricular systole. In contrast, nine patients with little or no change in the pressure gradient (residual basal gradient greater than or equal to 40 mm Hg) demonstrated a less marked decrease in septal thickness and no significant change in septal to mitral valve distance or magnitude of mitral systolic anterior motion. Furthermore, the postoperative left ventricular outflow tract area was significantly smaller in patients with residual basal gradients (3.0 +/- 1 cm2) than that in patients with no residual gradient (5.5 +/- 3 cm2; p less than .05). Ten patients with only provocable subaortic gradients after operation showed postoperative left ventricular outflow tract dimensions intermediate between those in patients with either residual basal gradient or no residual gradient. On the basis of this echocardiographic assessment of septal myotomy-myectomy, we conclude that abolition or reduction of the subaortic gradient after operation in patients with obstructive hypertrophic cardiomyopathy is largely the consequence of surgical enlargement of the left ventricular outflow tract area.
Automated impedance-based energy adjustment for defibrillation: experimental studies.
Authors: Kerber R E , McPherson D , Charbonnier F , Kieso R , Hite P
Published: June 2011

In defibrillation, current flow depends on the energy selected and the transthoracic impedance. If transthoracic impedance is high, current flow may be inadequate to defibrillate. We developed a method by which high transthoracic impedance is automatically compensated for by an increase in operator-selected energy when impedance is high. Transthoracic impedance was predicted in advance of the first shock by passing a low-level current between the defibrillator electrodes during the defibrillator charge cycle; a microprocessor monitored current flow and determined impedance. In 28 mongrel dogs we manipulated transthoracic impedance by placing glycerin-soaked gauze pads between the paddle electrodes and the chest. If the predicted impedance exceeded a preset value, the delivered energy was automatically increased by 40% or 100%. Using this impedance-based energy adjustment technique, we found significant improvements in current flow and success rate of shocks when energy was automatically increased to compensate for high transthoracic impedance. The use of transthoracic impedance as a basis for energy adjustment appears a promising technique to minimize the hazards of high electrical energy; it allows low-energy shocks in most patients while avoiding inappropriate low energies in patients with high impedance. Clinical trials are justified.
Persistent responsiveness of the neonatal ductus arteriosus in immature lambs: a possible cause for reopening of patent ductus arteriosus after indomethacin-induced closure.
Authors: Clyman R I , Campbell D , Heymann M A , Mauray F
Published: June 2011

Reopening of the ductus arteriosus after successful indomethacin-induced closure has become a major problem with indomethacin treatment. In full-term human newborns and lambs, the ductus behaves like ischemic tissue after its initial constriction. Its ability to continue to relax or contract depends on the amount of left-to-right shunt through the ductus lumen. To see if ductus constriction in preterm lambs would produce the same loss of ductus responsiveness, we delivered 42 lambs by cesarean section and ventilated them for 6.6 +/- 0.5 (+/- SE) hr. We measured ductus arteriosus resistance and left-to-right shunt with the use of radionuclide-labeled microspheres. After the hemodynamic measurements were obtained, the ductus was studied in vitro. Immature lambs were more likely to have reactive ductus (after their initial ductus constriction) than were more mature lambs. This was due to a diminished degree of ductus constriction as well as persistence of ductus responsiveness in immature lambs when compared with more mature lambs. This persistence of ductus responsiveness in immature lambs after ductus constriction may account for the high reopening rate in preterm infants after successful indomethacin-induced closure.
Effect of diltiazem and propranolol on left ventricular segmental relaxation during temporary coronary arterial occlusion and one month reperfusion in conscious dogs.
Authors: Tilton G D , Bush L R , Apprill P G , Buja L M , Willerson J T
Published: June 2011

Using sonar microcrystals implanted in conscious dogs, we have characterized left ventricular segmental relaxation (LVSR) by measuring the mean rate to half end-diastolic thinning (RHEDT) and the late diastolic thinning fraction (TF). In protocol 1 (five nonischemic dogs), RHEDT correlated with changes in left ventricular dP/dt (r = .87) and systemic arterial pressure (r = -.80) but not with alterations in heart rate. Only systemic arterial pressure importantly influenced TF (r = -.65). In protocol 2 (21 dogs), LVSR paralleled net systolic segmental wall thickness (NET) during both 2 and 4 hr of coronary occlusion followed by 1 month reperfusion. Both LVSR and NET remained depressed during 2 and 4 hr of coronary occlusion and through 24 hr of reperfusion, but both also gradually improved afterwards. In protocol 3, 31 dogs underwent 4 hr of coronary occlusion with 1 month of reperfusion. Among these animals, 11 dogs (group S4) received saline after 1 hr of occlusion, nine dogs (group P4) received propranolol, and 11 dogs (group D4) received diltiazem. Drug therapy was stopped at 2 hr of reperfusion. In segments with mildly and moderately depressed NET, LVSR was significantly increased in group D4 vs group S4 animals during the diltiazem infusion. Expressed as mean percentage of control value +/- SEM, RHEDT of moderately dysfunctional segments in group D4 compared with group S4 measured 53 +/- 10% vs 25 +/- 5%, respectively, at 2 hr of occlusion of the left anterior descending coronary artery (p = .03), 76 +/- 17% vs 28 +/- 8%, respectively, at 4 hr of occlusion (p = .01), and 74 +/- 11% vs 33 +/- 10%, respectively, at 1 hr of reperfusion (p less than .05). The differences in TF at these same time points were 106 +/- 10% vs 70 +/- 9% (p less than .03), 105 +/- 7% vs 65 +/- 16% (p less than .02), and 106 +/- 11% vs 74 +/- 13% (p less than .05), respectively. The improvement in LVSR occurred independently of changes in NET. The values of LVSR in the diltiazem-treated dogs fell to the levels of groups S4 and P4 within 24 hr of stopping the intervention. Propranolol did not significantly alter LVSR over the short or long term. The increase in LVSR during administration of diltiazem did not appear to be mediated by changes in contractility or regional myocardial blood flow, but were probably mediated in part by afterload reduction and possibly by a reduction in calcium entry into ischemic myocardium.
Effect of bepridil in patients with chronic stable angina: results of a multicenter trial.
Authors: Hill J A , O'Brien J T , Alpert J S , Gore J M , Zusman R M , Christensen D , Boucher C A , Vetrovec G , Borer J S , Friedman C
Published: June 2011

The effects of bepridil, a calcium antagonist with a half-life of approximately 42 hr, were assessed in a double-blind, randomized, placebo-controlled crossover trial. Forty-four patients (39 men, five women) with exercise-induced angina pectoris and ST segment depression with exercise testing (modified Bruce protocol) were studied. Compared with placebo bepridil (400 mg daily) increased total exercise time, time to onset of angina, time to 1 mm of ST segment depression, time to 2 mm of ST segment depression, and total work achieved (all p less than or equal to .001). Both frequency of angina and nitroglycerin consumption decreased during the bepridil compared with the placebo period (p = .02 and .03, respectively). Minor side effects were noted during both the bepridil and placebo phases. Four patients experienced side effects that limited therapy (dizziness in three and abnormal results of liver function tests in one) and one patient died during the bepridil phase. This study suggests that bepridil, 400 mg daily, is effective for the treatment of exercise-induced myocardial ischemia and angina pectoris.
Linking: a dynamic electrophysiologic phenomenon in macroreentry circuits.
Authors: Lehmann M H , Denker S , Mahmud R , Addas A , Akhtar M
Published: June 2011

The term "linking" has been used specifically to describe the mechanism for perpetuation of functional anterograde bundle branch block: namely, repetitive transseptal retrograde concealed penetration by impulses propagating along the contralateral bundle. We present selected examples that demonstrate tht linking-type phenomena actually have a wide spectrum of expression in human macroreentry circuits, particularly those incorporating either the bundle branches and His bundle or the normal pathway and Kent bundle. The examples presented are as follows: (1) persistent retrograde functional conduction delays in the His-Purkinje system during right ventricular pacing, (2) anterograde Kent bundle condution at rapid rates, dependent on prior block in the normal pathway, (3) persistent anterograde functional infra-His block of atrial impulses during rapid ventricular pacing in the presence of a retrogradely conducting accessory pathway, and (4) transient advancement of His activation with ventricular fusion complexes during overdrive ventricular pacing of bundle branch reentrant tachycardia. Based on these examples, we characterize linking as a generalized electrophysiologic phenomenon in which each successive impulse entering a macroreentry circuit propagates preferentially along one limb because of functional block in the contralateral limb resulting from the effects of the prior impulse. It is proposed that such functional block may be dynamically maintained either by repetitive impulse interference, which perpetuates local refractoriness (examples No. 1 to 3), or by repetitive impulse collision (example No. 4). The general conceptual scheme outlined can be applied to specific electrophysiologic phenomena associated with a wide variety of reentry circuits in man.
Left ventricular chamber filling and midwall fiber lengthening in patients with left ventricular hypertrophy: overestimation of fiber velocities by conventional midwall measurements.
Authors: Shimizu G , Zile M R , Blaustein A S , Gaasch W H
Published: June 2011

Observations that the inner (subendocardial) half of the left ventricular wall contributes more to total left ventricular wall thickening than the outer (subepicardial) half may have important implications in the analysis of myocardial fiber length transients. Accordingly, we measured endocardial and midwall shortening and lengthening rates in normal and hypertrophic heart and compared the results obtained with conventional methods of measurement with those obtained with a modified model that does not depend on use of conventional assumptions about the midwall. This modified (two-shell) cylindrical model) method considers the substantial contribution of inner wall thickening and thus does not require the assumption of a theoretical midwall fiber that remains at the midwall throughout the cardiac cycle. Echocardiographic data from six normal subjects and six patients with concentric left ventricular hypertrophy (LVH) were examined; left ventricular wall thickness ranged from 8 to 10 mm in normal subjects and from 11 to 16 mm in the patients with LVH. By design, the standard measurements of left ventricular size (diastolic and systolic dimensions) and systolic function (fractional shortening and endocardial fiber shortening velocities) were equal in the two groups. Endocardial, conventional midwall, and modified midwall methods all indicate reduced fiber lengthening rates in patients with LVH; peak fiber lengthening rates for normal and LVH groups were 4.5 +/- 0.7 vs 3.1 +/- 0.8 sec-1 (p less than .02) at the endocardium, 2.3 +/- 0.4 vs 1.6 +/- 0.4 sec-1 (p less than .02) at the midwall (conventional method), and 2.1 +/- 0.3 vs 1.4 +/- 0.3 sec-1 (p less than .01) at the midwall (modified method).(ABSTRACT TRUNCATED AT 250 WORDS)
Academic-industrial relationships.
Authors: Sanders C A
Published: June 2011

In conclusion, it is obvious that the delivery system for medical care is changing much faster than anticipated. Technology is the agent in this process and economics is both the driving and the limiting force: driving because it is the impetus to change the sites of medical practice, limiting because of the constrained number of dollars to allocate to technology acquisition and operation. As we move into the future, it cannot be emphasized too strongly that hospitals and industry should be complementary in this process. To do so successfully requires an understanding of the mission each seeks to pursue and of what each can do for the other.
Contribution of left ventricular contraction to the generation of right ventricular systolic pressure in the human heart.
Authors: Feneley M P , Gavaghan T P , Baron D W , Branson J A , Roy P R , Morgan J J
Published: June 2011

To determine whether left ventricular (LV) contraction contributes to the generation of right ventricular (RV) systolic pressure in humans, LV and RV pressures and their first derivative (dP/dt) were recorded simultaneously with micromanometer-tipped catheters in 11 conscious subjects. Seven subjects had normal LV and coronary angiograms. Four subjects had moderate LV dysfunction (resting ejection fraction 0.40 to 0.50), and three of these had coronary artery disease. During normal sinus rhythm, LV contraction slightly preceded RV contraction (mean 20 msec), and LV and RV dP/dt recordings showed single positive systolic peaks that were coincident. During endocardial pacing of the RV free wall, RV contraction preceded LV contraction (mean 23 msec) and two systolic RV dP/dt peaks were recorded, the first (peak I) occurring significantly before (mean +/- SD = 67 +/- 23 msec, p less than .01), and the second (peak II) coincident with the single systolic LV dP/dt peak. RV ectopic beats produced a similar RV dP/dt pattern, with peak I occurring 63 +/- 11 msec (p less than .01) before, and peak II coincident with the single LV dP/dt peak. Conversely, during LV ectopic beats, LV contraction preceded RV contraction (mean 63 msec) and two systolic RV dP/dt peaks were recorded, but peak I was coincident with the single LV dP/dt peak, while peak II occurred significantly later (63 +/- 26 msec, p less than .01). In two subjects right bundle branch block produced similar findings. In three subjects left bundle branch block produced little ventricular asynchrony (mean 14 msec), but did delay the development of peak LV dP/dt after LV contraction.(ABSTRACT TRUNCATED AT 250 WORDS)
Increased forearm vascular reactivity in patients with hypertension after repair of coarctation.
Authors: Gidding S S , Rocchini A P , Moorehead C , Schork M A , Rosenthal A
Published: June 2011

To determine whether altered vascular reactivity could contribute to hypertension after repair of coarctation, the change in forearm and calf vascular resistances to small intra-arterial infusions of norepinephrine were measured in six patients who had undergone surgical correction of coarctation of the aorta but still had upper extremity hypertension and compared with similar measurements made in five normotensive patients with mild heart disease. Only the mean upper extremity pressure was significantly greater in the group that underwent repair of coarctation (102 +/- 11 vs 83 +/- 5 mm Hg, p less than .05, for mean arm pressures and 96 +/- 13 vs 83 +/- 7 mm Hg for mean leg pressures in patients who had coarctation vs normotensive patients, respectively). Forearm and calf blood flows were measured in the right arm and leg with a mercury-in-plastic strain-gauge plethysmograph. Forearm and calf vascular resistances were calculated by dividing mean arterial pressure of the appropriate extremity by the blood flow of that extremity. Norepinephrine was infused into the right brachial and femoral arteries of the patients at doses of 0.02, 0.05, 0.1, 0.2, 0.3, 0.5, and 0.7 microgram/min. Resting forearm and calf vascular resistances were similar in both groups of patients. The norepinephrine dose-response curves showed that control patients required more than three times the norepinephrine to produce the same percent increase in forearm vascular resistance (after 0.2 microgram/min forearm vascular resistance increased by 55% in the coarctation group, while the resistance in the control group increased by only 3%, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
Transcatheter ablation: comparison between laser photoablation and electrode shock ablation in the dog.
Authors: Lee B I , Gottdiener J S , Fletcher R D , Rodriguez E R , Ferrans V J
Published: June 2011

To characterize and compare the effects of transcatheter laser and electrical energy on endocardium, 35 laser pulses were delivered to the endocardial surfaces of isolated canine hearts, and 33 endocardial lesions were produced by the transarterial delivery of either transcatheter laser irradiation or electrical shock in closed-chest anesthetized dogs. Laser-induced lesion dimensions in vitro and in vivo increased with increased total dose of energy; however, the lesions produced in vivo were different in morphology and were significantly larger than lesions produced by equivalent doses of energy delivered in vitro (p less than .05). Endocardial lesions produced in vivo by laser at 40 and 80 J (7.9 X 5.4 X 6.6 and 7.9 X 5.1 X 7.5 mm) were comparable in gross morphology and size to those produced by electrical shock at 100 and 200 J (8.5 X 6.6 X 6.6 and 10.0 X 8.5 X 8.2 mm, respectively; p = NS), but transcatheter electrode shock produced significantly more ventricular tachycardia (p less than .003), premature ventricular beats in the 7 min after energy discharge (p less than .05), and wall motion abnormality (p less than .005). Transcatheter laser photoablation can create controlled endocardial lesions with less energy and fewer deleterious effects than transcatheter electrode shock.
Early detection of canine myocardial infarction by magnetic resonance imaging in vivo.
Authors: Pflugfelder P W , Wisenberg G , Prato F S , Carroll S E , Turner K L
Published: June 2011

This study was undertaken to assess the ability of proton magnetic resonance imaging (MRI) to detect myocardial ischemia shortly after coronary artery occlusion. Fifteen dogs were studied before and serially for up to 6 hr after anterior descending or circumflex coronary artery ligation in vivo by gated MRI with a 0.15 tesla resistive magnet (resonant frequency of hydrogen 6.25 MHz). Image acquisition was by single-spin echo, with echo times (TE) of 30 msec and TE 60 msec, and modified inversion recovery pulse sequences. Excellent anatomic definition was observed. By 4 hr after coronary artery occlusion the signal in the infarct zone increased to 36 +/- 20% greater than that in the adjacent normal myocardium for the TE 30 msec sequence (p less than .01) and to 116 +/- 100% for the TE 60 msec sequence (p less than .05). The most intense increase in signal was noted with the TE 60 msec pulse sequence and because normal myocardium is not well visualized by this technique, acutely ischemic myocardium was clearly delineated. Inversion recovery imaging did not show areas of ischemia. Changes seen on MR images correlated well with the location of ischemic changes noted on microscopic examination of the excised hearts. MRI thus provides a noninvasive means for detection of ischemia early in the course of myocardial infarction.
Hemodynamic findings at rest and during mild supine exercise in adults with isolated, uncomplicated ventricular septal defects.
Authors: Otterstad J E , Simonsen S , Erikssen J
Published: June 2011

Fifty-two patients with isolated congenital ventricular septal defects (VSDs), studied for the first time at age 10 or older, were restudied an average of 16 years later (range 4 to 21). The study protocol included a symptom-limited bicycle ergometer test, M mode echocardiographic examination, and hemodynamic studies at rest and during mild supine exercise. Of the 52, 17 had been operated on an average of 19 years earlier (range 11 to 21) (group 1) and 35 with smaller defects were not operated on (group 2). Although more pronounced findings were made in group 1, a similar pattern was observed in group 2: In most subjects in both groups a subnormal working capacity was observed. A subnormal left ventricular fractional shortening and circumferential shortening velocity was noted in a high proportion at echocardiography. A number of hemodynamic aberrations were observed in a high proportion of patients during exercise but not at rest. Thus a subnormal increase in left and right ventricular cardiac output was found in addition to pathologic increase in right and left ventricular end-diastolic, pulmonary arterial, and pulmonary capillary wedge pressures. In group 1, elevated pulmonary arterial pressures before operation and/or small residual VSDs were associated with a poor hemodynamic outcome. In neither group could significant correlations be observed between hemodynamic aberrations, shunt size, and/or age. Among patients who underwent surgery, the earlier surgical trauma might have contributed to the functional aberrations, but in group 2 the only likely explanation for the findings seems to be the VSD itself. Possibly a long-standing VSD--found unnecessary to repair according to commonly accepted criteria--may lead to disturbed systolic function and increase in compliance of both ventricles via a chronic pressure and volume overload.
Elevation of brachial arterial blood velocity and volumic flow mediated by peripheral beta-adrenoreceptors in patients with borderline hypertension.
Authors: Levenson J , Simon A C , Safar M E , Bouthier J D , London G M
Published: June 2011

Simultaneous determinations of cardiac output and brachial arterial blood flow were performed in patients with hypertension and high cardiac output in comparison with normal subjects of the same age. Brachial arterial blood flow was measured with a previously described pulsed Doppler apparatus that permitted the noninvasive determination of arterial diameter and blood flow velocity. In patients with borderline hypertension, brachial blood flow was significantly increased (136 +/- 11 vs 72 +/- 8 ml/min; p less than .001). After short-term administration of indomethacin, cardiac output decreased while brachial blood flow remained constant. After short-term administration of a selective beta 1-receptor antagonist (primidolol) and nonselective blocker (propranolol), cardiac output decreased significantly in both cases but the decrease in brachial blood flow was significant only after the administration of the nonselective beta-blocking agent. The study strongly suggested that in patients with borderline hypertension, the increased cardiac output is related to a prostaglandin and beta 1-adrenergic mechanisms whereas the increased brachial blood flow depends mainly on beta 2-adrenergic mechanisms.
Tiapamil, a new calcium antagonist: hemodynamic effects in patients with acute myocardial infarction.
Authors: Eichler H G , Mabin T A , Commerford P J , Lloyd E A , Beck W , Opie L H
Published: June 2011

The afterload reduction and myocardial oxygen sparing that results after administration of calcium antagonists suggests a possible role for these drugs in intervention after onset of acute myocardial infarction, but their use in this setting is limited by the possibility that left ventricular failure will develop. Tiapamil is a new verapamil congener. The hemodynamic effects of this drug (1 mg/kg followed by 25 micrograms/kg/min over 36 hr) were studied in 30 patients randomly assigned in a double-blind manner to a tiapamil or control group within 12 hr of the onset of acute myocardial infarction as diagnosed by Swan-Ganz catheterization and gated blood pool scans. Tiapamil reduced heart rate from 83 +/- 20 beats/min (mean +/- SD) before to 74 +/- 19 beats/min after drug (over an average 36 hr), arterial pressure from 128 +/- 22/87 +/- 14 to 118 +/- 16/74 +/- 11 mm Hg, rate-pressure product from 10,695 +/- 3492 to 8800 +/- 2550 units, and systemic vascular resistance from 1732 +/- 351 to 1400 +/- 350 dynes X sec X cm-5. Tiapamil also increased stroke volume index from 34.7 +/- 12.1 to 41.6 +/- 12.0 ml/m2, left ventricular ejection fraction from 50.1 +/- 14.8% to 56.4 +/- 17.4% (at 24 hr), left ventricular end-diastolic volume index from 71.3 +/- 23.1 to 80.5 +/- 23.7 ml/m2, and peak diastolic filling rate (an index of diastolic relaxation) from 2.1 +/- 0.9 to 2.6 +/- 0.8 end-diastolic volumes/sec (p less than .05 for all changes). Cardiac index, wedge pressure, left ventricular end-systolic volume, and PR interval remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Long-term results, hemodynamics, and complications after combined heart and lung transplantation.
Authors: Dawkins K D , Jamieson S W , Hunt S A , Baldwin J C , Burke C M , Morris A , Billingham M E , Theodore J , Oyer P E , Stinson E B
Published: June 2011

During the first 31/2 years of the Stanford heart-lung transplant program, 23 transplants have been carried out in 22 patients with severe pulmonary vascular disease. Actuarial survival curves predict 1 and 2 year survival rates of 71% and 57%, respectively, for all patients. As a result of increasing experience, the early mortality of 26% has been reduced, with only one early death occurring in the last eight patients; prior cardiac surgery was a contributing factor in three of the six patients suffering early deaths. Two late deaths occurred in the series 14 and 15 months after operation. One patient died suddenly as a result of an acute myocardial infarct and the other patient died because of respiratory failure. At autopsy, both patients had severe proliferative coronary atherosclerosis with obliterative bronchiolitis affecting the lungs. An additional patient required a retransplant for obliterative bronchiolitis 37 months after the initial procedure, and he too was found to have severe coronary artery disease. Hemodynamics and left ventricular function were normal in patients studied 1 and 2 years after undergoing the transplantation procedure. Thus, the early mortality and morbidity of combined heart and lung transplantation has been significantly reduced, but the long-term complications, particularly graft atherosclerosis and obliterative bronchiolitis, are yet to be fully controlled.
Increase in myocardial oxygen consumption indexes by exercise training at onset of ischemia in patients with coronary artery disease.
Authors: Laslett L J , Paumer L , Amsterdam E A
Published: June 2011

It has been unclear whether exercise training of patients with coronary artery disease increases the level of myocardial oxygen consumption, as indicated by heart rate and double product of heart rate and systolic blood pressure, at which electrocardiographic evidence of myocardial ischemia develops. To assess this question we evaluated the experience of 10 patients with coronary artery disease who underwent a modest-level exercise training program for 6 months. All of these subjects had achieved a training effect, had developed electrocardiographic evidence of ischemia during initial exercise testing, had not increased the amount of cardiac medication taken, and had not been taking digoxin. After completion of the training period, the mean heart rate at which electrocardiographic evidence of ischemia developed increased from 107 +/- 19 to 119 +/- 23 beats/min (p less than .05) and the mean double product increased from 166 +/- 18 to 209 +/- 51 X 10(2) mm Hg X beats/min (p less than .05). Eight of the 10 patients demonstrated an increase in heart rate at onset of ischemia (p less than .02), and seven of the eight in whom double product could be assessed manifested an increase in this parameter at onset of ischemia (p less than .05). Thus the rate of myocardial oxygen consumption at which myocardial ischemia develops, as indirectly assessed by heart rate and double product, can be favorably altered by 6 months of moderate-level exercise training.
Factors that determine recovery of left ventricular function after thrombolysis in patients with acute myocardial infarction.
Authors: Sheehan F H , Mathey D G , Schofer J , Dodge H T , Bolson E L
Published: June 2011

The coronary and ventricular angiograms of 47 patients with acute myocardial infarction in whom reperfusion was achieved by intracoronary streptokinase were quantitatively analyzed to determine the factors that affect recovery of regional left ventricular function after reperfusion. Hypokinesis in the infarct region was measured by the centerline method and expressed in terms of standard deviations (SDs) from normal. Severity of coronary artery stenosis was measured quantitatively. Hypokinesis showed more significant improvement after thrombolysis in patients with minimum stenosis diameter of greater than 0.4 mm than in those with severe residual stenosis, i.e., stenosis producing a minimum diameter of 0.4 mm or less (1.0 +/- 1.3 SD/chord, n = 31, vs 0.0 +/- 0.9 SD/chord, n = 7; p less than .05). Improvement in hypokinesis was greater in patients who received thrombolytic therapy within 2 hr than in those treated later (2.1 +/- 1.1, n = 8, vs 0.7 +/- 1.0 SD/chord, n = 28; p less than .001). These results indicate that angiographic reperfusion alone may not be sufficient: reperfusion must provide adequate flow and be achieved early to salvage myocardial function.
Platelet activation and secretion associated with emotional stress.
Authors: Levine S P , Towell B L , Suarez A M , Knieriem L K , Harris M M , George J N
Published: June 2011

Platelets are believed to play a role in the pathogenesis of atherosclerosis and of the vascular obstruction that causes the acute complications of coronary artery disease. Since specific behavioral patterns appear to be related to the development of coronary artery disease and since emotional stress may predispose an individual to acute cardiovascular ischemia, it was hypothesized that platelet activation by catecholamines might be involved in these events. To study emotional stress, plasma samples were obtained from 61 senior medical residents immediately before they were to speak in public. There were significant increases in the plasma concentrations of the platelet-secreted proteins platelet factor 4 and beta-thromboglobulin and epinephrine and norepinephrine immediately before speaking, which demonstrates that platelet activation and secretion occur in association with this type of emotional stress. Four trials were carried out to study the mechanism for this observed platelet secretion: (1) phenoxybenzamine, (2) propranolol, (3) 650 mg aspirin, and (4) 80 mg aspirin were given several hours before the public speaking engagement. Neither phenoxybenzamine nor propranolol in doses that blocked the hemodynamic effects of alpha 1- and beta 1-adrenergic stimulation modified platelet secretion. Aspirin also did not block platelet secretion, which suggests that platelets were not being stimulated through a cyclooxygenase-dependent pathway. This study provides direct evidence of platelet secretion in vivo in association with emotional stress, and underscores the potential importance of platelet activation and secretion in the acute events that occur in patients with vascular disease.
Cardiac causes of shock early after open heart surgery: etiologic classification by radionuclide ventriculography.
Authors: Bateman T M , Czer L S , Kass R M , Raymond M J , Chaux A , Matloff J M , Berman D S , Gray R J
Published: June 2011

Early after open heart surgery, cardiac shock due to tamponade is easily misdiagnosed as ventricular dysfunction. The distinction is critical to successful therapy. We assessed the utility of 99mTc-red blood cell, gated equilibrium radionuclide ventriculography in 50 patients with early postoperative cardiac shock after historical, clinical, and invasive hemodynamic evaluation failed to identify either tamponade or ventricular dysfunction as the specific cause of their shock. The cause was established by radionuclide ventriculography in 45 of 50 patients and led to a change in therapy in 21 patients. A single cause was found in 35 patients: 13 had severe global dysfunction of the left ventricle (three patients), right ventricle (seven patients), or both ventricles (three patients); three had severe segmental left ventricular dysfunction; and 19 had an exaggerated region of photon deficiency (nine patients) or an abnormal and accumulating blood pool (10 patients) surrounding small hyperdynamic ventricles. Sixteen of these 19 patients with scintigraphic evidence of tamponade underwent aspiration with a pericardial needle or reoperation early after radionuclide ventriculography, resulting in confirmation of scintigraphic findings and improved hemodynamics. Ten additional patients had combined ventricular dysfunction and a pericardial abnormality, and five of these underwent reoperation resulting in improved hemodynamics. Radionuclide ventriculography provided no explanation for the cause of cardiac shock in five patients. Thus, the various causes of cardiac shock early after open heart surgery can be distinguished by 99mTc-red blood cell, gated equilibrium radionuclide ventriculography, eliminating diagnostic uncertainty that can occur with traditional evaluation.
Enhancement of the antiaggregatory activity of prostacyclin by propranolol in human platelets.
Authors: Callahan K S , Johnson A R , Campbell W B
Published: June 2011

The beta-adrenergic antagonist propranolol has been found to inhibit platelet aggregation. We investigated the possibility that propranolol exerts this action by stimulating the synthesis or enhancing the antiaggregatory activity of prostaglandin (PG) I2. The media from cultures of human endothelial cells inhibited thrombin-induced platelet aggregation, an effect attributed to PGI2 production by the cells. When endothelial cells were incubated with dl- or d-propranolol, the media had two to three times the inhibitory activity of control media. However, this increased activity was not due to increased synthesis of PGI2 because control and propranolol-treated cultures synthesized similar amounts of the PGI2 metabolite, 6-keto-PGF1 alpha. Instead, propranolol enhanced the antiaggregatory activity of PGI2. Propranolol (1 microM) and PGI2 (0.05 nM), when tested separately, inhibited aggregation by 19% and 13%, respectively, whereas the combination inhibited aggregation by 51%. PGI2 inhibited platelet aggregation and thromboxane (Tx) B2 production but stimulated cyclic AMP formation. The adenyl cyclase inhibitor 2',5'-dideoxyadenosine (DDA) had no effect of its own on these parameters, but blocked the actions of PGI2. Propranolol inhibited aggregation and TxB2 synthesis without changing cyclic AMP levels. Unlike PGI2, propranolol's effects were not altered by DDA. While the combination of propranolol and PGI2 inhibited aggregation to a greater extent than either agent alone, this enhanced effect with the combination did not extend to TxB2 or cyclic AMP production. Propranolol, PGI2, and the combination inhibited TxB2 synthesis to a similar extent, and PGI2 produced a similar increase in cyclic AMP in the presence and absence of propranolol. These findings indicate that propranolol and PGI2 inhibit platelet aggregation through cyclic AMP-independent and dependent mechanisms, respectively. While propranolol does not alter the synthesis of PGI2, it enhances the inhibition of aggregation by PGI2, and this may contribute to its antiplatelet effect.
Day-to-day variations in inducibility of ventricular tachyarrhythmias during the late postmyocardial infarction phase in conscious dogs.
Authors: Cobbe S M , Hoffmann E , Ritzenhoff A , Brachmann J , Kübler W , Senges J
Published: June 2011

The inducibility of ventricular tachyarrhythmias was studied daily on days 3 through 8 after experimental myocardial infarction in 15 conscious dogs. Although a sustained ventricular tachyarrhythmia was produced on one or more occasions in 11 of 15 dogs (73%), there was marked daily variation in the results of programmed stimulation. Ventricular fibrillation or sustained ventricular tachycardia was elicited in six dogs on day 3 after infarction. In two of these dogs, no sustained tachycardia could be induced by day 7. In nine dogs sustained ventricular arrhythmias were not inducible on day 3. By day 6 to 7, sustained ventricular tachycardia was inducible in five of these dogs. In clinical practice similar variation in the inducibility of sustained ventricular arrhythmias may conceivably complicate the use of results of programmed ventricular stimulation as determinants of risk of sudden death after myocardial infarction.
Fibrin formation and platelet aggregation in patients with severe coronary artery disease: relationship with the degree of myocardial ischemia.
Authors: Gallino A , Haeberli A , Baur H R , Straub P W
Published: June 2011

Fibrinopeptide A (FpA) concentrations in plasma and in 24 hr urine specimens as well as beta-thromboglobulin (BTG) in plasma were measured in 17 patients with severe angina pectoris, including both stable and unstable angina, and in 19 patients with acute myocardial infarction. Patients with unstable angina had plasma FpA and BTG levels of 5.2 +/- 1.7 ng/ml and 91 +/- 23 ng/ml, respectively. The corresponding concentrations of FpA in the 24 hr urine specimens were 8.2 +/- 1.4 micrograms/24 hr. These values were similar to those measured in patients with acute myocardial infarction and higher than the corresponding levels in patients with stable angina (p less than .05) and in normal control subjects (p less than .01). The similarity of the platelet and coagulation findings in patients with unstable angina and in those with myocardial infarction favors the hypothesis that coronary thrombosis may play a major role in the pathogenesis of acute myocardial infarction.
Participation of endogenous catecholamines in the regulation of left ventricular mass in progeny of hypertensive parents.
Authors: Trimarco B , Ricciardelli B , De Luca N , De Simone A , Cuocolo A , Galva M D , Picotti G B , Condorelli M
Published: June 2011

To investigate whether adrenergic activity is a determinant of left ventricular hypertrophy in human hypertension, in each of 10 normotensive subjects with two hypertensive parents we have examined the relationship between changes in echocardiographic parameters of left ventricular anatomy and those in circulating catecholamine levels induced by three, 3 week periods of different sodium and potassium intakes. A high sodium-normal potassium regimen induced a significant reduction in upright plasma norepinephrine (from 599 +/- 89 to 379 +/- 45 pg/ml, p less than .01) and in posterior wall (PWT) and interventricular septal (IVST) thickness, as well as in the left ventricular mass index (LVMi). Changes in upright plasma norepinephrine concentrations correlated with those in IVST (r = .822, p less than .01) and in LVMi (r = .833, p less than .01). A low sodium-normal potassium diet resulted in increases in supine and upright plasma norepinephrine levels (from 356 +/- 44 to 488 +/- 89 pg/ml, p less than .001; and from 565 +/- 42 to 744 +/- 33 pg/ml, p less than .01) as well as increases in IVST and LVMi (from 97 +/- 7 to 107 +/- 7 g/m2, p less than .001). The changes in norepinephrine levels in supine and upright subjects correlated with changes in IVST (r = .836, p less than .01 and r = .796, p less than .01) and in LVMi (r = .931, p less than .001 and r = .947, p less than .001). No significant change in plasma catecholamine concentrations or in PWT, IVST, or LVMi was detected after a low sodium-high potassium regimen.(ABSTRACT TRUNCATED AT 250 WORDS)
Transient enhancement of sympathetic nervous system activity by long-term restriction of sodium intake.
Authors: Volpe M , Müller F B , Trimarco B
Published: June 2011

To further investigate the relationship between salt intake and sympathetic nervous system activity, the short- and long-term effects of a low-salt diet (40 meq/day) were assessed in 10 normal subjects. Measurements of hemodynamic, hormonal, and other parameters were obtained on the day preceding institution of the low-salt diet (day 0) and on days 4, 7, 30, and 60 of the diet. Urinary sodium excretion was 178 +/- 10 meq/24 hr on day 0 and 31 +/- 4, 38 +/- 4, 45 +/- 6, and 47 +/- 7 meq/24 hr on days 4, 7, 30, and 60, respectively (all p less than .001 compared with day 0). Blood pressure, urinary potassium, serum electrolytes, and cardiac function (as assessed by echocardiography) were not modified by the 2 month low-salt diet. Plasma renin activity and plasma aldosterone were significantly elevated above control values throughout the entire period of the low-salt diet. In contrast, plasma norepinephrine concentration increased significantly only on days 4 and 7 (from 253 +/- 20 pg/ml on day 0 to 495 +/- 32 pg/ml, p less than .001, and 347 +/- 22 pg/ml, p less than .05, respectively), returning to baseline at days 30 (280 +/- 18 pg/ml) and 60 (262 +/- 18 pg/ml). Changes in plasma epinephrine paralleled those observed for norepinephrine. Similarly, resting heart rate and the blood pressure response to isometric exercise were significantly increased only on days 4 and 7 of the low-salt diet. These results suggest that sympathetic nervous system activity is enhanced only transiently during a sustained reduction in sodium intake.
Mildly dilated congestive cardiomyopathy.
Authors: Keren A , Billingham M E , Weintraub D , Stinson E B , Popp R L
Published: June 2011

Five patients with only mildly dilated ventricles but other features typical of congestive cardiomyopathy underwent cardiac transplantation for class IV NYHA heart failure. The findings of clinical studies, cardiac catheterization, endomyocardial biopsy, and pathologic examination of the removed hearts in this group with mildly dilated congestive cardiomyopathy (MDCM) were compared with similar data in four patients with idiopathic restrictive cardiomyopathy (IRCM) and in 10 patients with typical dilated congestive cardiomyopathy (DCM). In comparison with the other groups, patients with MDCM had a higher incidence of familial cardiomyopathy (p = .02) and a shorter symptomatic period than patients with IRCM (p less than .02). Patients with both MDCM and DCM had globular hearts (with predominant left ventricular dilatation), congestive hemodynamics and poor left ventricular contractility (ejection fraction 12% to 19%), and high incidence of ventricular thrombi. Patients with IRCM showed normal ventricular size, marked atrial dilatation, restrictive hemodynamics, mild-to-moderate decrease in left ventricular contractility (ejection fraction 29% to 55%), and absence of ventricular thrombi. Cardiac index, ventricular wall thickness, and light microscopic findings were similar in the three groups of patients. Electron microscopy showed no myofibrillar loss in patients with IRCM but mild (partial) or moderate-to-severe (almost total) myofibrillar loss in those with MDCM and DCM, respectively. We conclude that end-stage congestive cardiomyopathy may occur without significant ventricular dilatation and patients with MDCM have heart sizes intermediate between those found in IRCM and DCM but their clinical, hemodynamic, and pathologic findings are virtually identical to those of patients with typical DCM.
A Doppler-two-dimensional echocardiographic method for quantitation of mitral regurgitation.
Authors: Ascah K J , Stewart W J , Jiang L , Guerrero J L , Newell J B , Gillam L D , Weyman A E
Published: June 2011

A noninvasive method to accurately quantitate the severity of mitral insufficiency would be of major clinical value. In theory, in the absence of confounding variables, regurgitant mitral flow should represent the difference between forward mitral blood flow and aortic blood flow. Since Doppler-two-dimensional echocardiographic (D2DE) methods for measuring transvalvular mitral and aortic flow have been validated, it should be possible to use mitral and aortic flows derived by this method to calculate regurgitant mitral flow. To assess the validity and accuracy of this combined approach for quantitation of regurgitant flow, we developed an open-chest canine preparation in which we could simulate, vary, and accurately measure degrees of mitral regurgitation. Seven animals were anesthetized and prepared to allow controlled right heart output. Mitral regurgitation was than simulated by placing a flexible conduit incorporating a one-way valve and electromagnetic flowmeter between the left ventricular apex and left atrium. Flow through the tube (effective mitral regurgitation) was varied between 0.2 and 1.8 liters/min and forward cardiac output ranged between 0.5 and 4 liters/min. Transmitral and transaortic flows were calculated by previously reported Doppler methods. Doppler-derived estimates of forward flow through the aortic valve correlated well with the flow measured by flowmeter (r = .92), and regurgitant flow and regurgitant fraction calculated by the D2DE approach also compared well with those measured by flowmeter (r = .84 and .83, respectively). This study demonstrates that mitral regurgitant flow and regurgitant fraction calculated by the D2DE method provide an acceptable measure of both absolute regurgitant flow and the regurgitant fraction in the experimental setting.