bluuebunny/crossref_metadata_2025 huggingface dataset:
The effects of pressure-induced right ventricular hypertrophy on left ventricular diastolic properties and dynamic geometry in the conscious dog.
Authors: Visner M S , Arentzen C E , Crumbley A J , Larson E V , O'Connor M J , Anderson R W
Published: June 2011

To determine whether chronic pressure overload and hypertrophy of the right ventricle alter the diastolic properties of the left ventricle, six adult dogs underwent banding of the pulmonary artery and were instrumented for studies 8 months later. Fourteen control dogs were also studied. Pressure and dimension data were collected from the dogs while they were awake and unsedated. The anterior-posterior, septal-free wall, and base-apex axis diameters of the left ventricle were measured with ultrasonic dimension transducers. Right and left ventricular pressures were measured with micromanometers. Pulmonary arterial banding resulted in increased right ventricular/body mass ratios (2.70 +/- 0.36 g/kg vs 1.52 +/- 0.15 g/kg control; p less than or equal to .05) and increased left ventricular/body mass ratios (4.84 +/- 0.64 g/kg vs 4.21 +/- 0.49 g/kg control; p less than or equal to .05). Right ventricular peak systolic and end-diastolic pressures were higher among the banded dogs (50 +/- 20/7 +/- 5 mm Hg vs 31 +/- 6/3 +/- 2 mm Hg control; p less than or equal to .05). A rearrangement in the three-dimensional geometry of diastolic filling occurred in the banded dogs. Extension from unstressed diastolic dimension (strain) in the base-apex axis was significantly larger in the banded dogs at left ventricular transmural pressures of 12, 8, and 4 mm Hg; strains in the septal-free wall axis were significantly smaller at transmural pressures of 12 and 8 mm Hg. Normalized diastolic left ventricular pressure-volume data and midwall circumferential stress-strain data were fit to the Kelvin viscoelastic equation. The normalized pressure-volume relationships of the banded dogs lay significantly to the left of those of the controls, indicating a loss of left ventricular chamber compliance. The midwall circumferential stress-strain relationships of the banded dogs were also shifted to the left, indicating a loss of intrinsic myocardial compliance. Thus, during the course of right ventricular hypertrophy caused by right ventricular pressure overload, alterations in the mass, geometry, and material properties of the left ventricle occur. At 8 months the chamber compliance of the left ventricle is compromised by these changes.
Comparative effects of nicardipine, a new calcium antagonist, on size of myocardial infarction after coronary artery occlusion in dogs.
Authors: Endo T , Nejima J , Fujita S , Kiuchi K , Iida N , Kikuchi K , Hayakawa H , Okumura H
Published: June 2011

To examine whether nicardipine, a dihydropyridine derivative, limits size of myocardial infarction, and to compare the protective effects of nicardipine administered before and early and late after coronary artery occlusion, 99mTc-labeled albumin microspheres were injected into the left atrium during 5 min temporary coronary artery occlusion to determine the extent of the hypoperfused zone (the area at risk). The coronary arteries were then reperfused for 45 min before 6 hr permanent coronary artery occlusion. Fifteen minutes before permanent occlusion, dogs were randomly assigned to a control group (n = 11), a pretreatment group (n = 9), which received at this point 10 micrograms/kg of nicardipine as a loading dose followed by a continuous infusion of 8 micrograms/kg/hr for 6 hr, an early treatment group (n = 9), in which nicardipine treatment was initiated 15 min after occlusion, or a late treatment group (n = 8), in which nicardipine administration was delayed for 3 hr. Six hours after coronary artery occlusion, the hearts were excised and the left ventricle of each was cut into 3 mm thick slices and stained with triphenyltetrazolium chloride. The extent of myocardial necrosis was measured by planimetry of the unstained areas. Thereafter, the same slices were autoradiographed and the extent of the hypoperfused zone was measured by planimetry of the "cold spot." The extent of the hypoperfused zone was identical among the four groups. In the control group, the ratio of the extent of myocardial necrosis to the extent of the hypoperfused zone was 95.8 +/- 3.8% (mean +/- SEM). However, it was significantly smaller in the pretreatment group (59.9 +/- 13.3%, p less than .05) and the early treatment group (49.0 +/- 10.6%, p less than .01) than in the control group. In the late treatment group, this value was not different from that in the control group (86.5 +/- 7.1%). There was a close inverse correlation between reduction of infarct size and the extent of the hypoperfused zone in the pretreatment and early treatment groups. Thus, nicardipine administered before or early after coronary artery occlusion limited infarct size by 37% to 49%, whereas when administration was delayed for 3 hr infarct size was not reduced. Furthermore, nicardipine had more striking effects on the ischemic myocardium of dogs with small hypoperfused zones than on that of dogs with large hypoperfused zones.
Endurance training in rats with chronic heart failure induced by myocardial infarction.
Authors: Musch T I , Moore R L , Leathers D J , Bruno A , Zelis R
Published: June 2011

The response to exercise was investigated in trained and sedentary rats with moderate compensated heart failure produced by myocardial infarction (MI) and in rats that underwent sham operations. Trained rats ran on a treadmill (10% grade at 20 m/min) for 60 min/day, 5 days/week for 10 to 12 weeks, whereas sedentary rats had only limited activity. Maximal oxygen consumption normalized for body weight (ml kg-1 min-1) was determined for each rat and found to be (1) greater in trained rats when compared with sedentary rats and (2) greater in sham-operated rats when compared with their counterparts that suffered infarction. In addition, skeletal muscle succinate dehydrogenase activities were greater and the blood lactic acid response to submaximal exercise was lower in trained rats compared with sedentary rats. Left ventricular infarct size for sedentary and trained rats with infarction was 36 +/- 3% and 34 +/- 3% of the total endocardial circumference, respectively, and resulted in (1) elevated left ventricular end-diastolic pressures at rest and during exercise, (2) lower mean arterial pressures at rest, and (3) lower maximal heart rates when compared with those in their sham-operated counterparts. However, normalization of mean arterial pressures during submaximal and maximal exercise was found along with a trend toward normalization of maximal heart rate when trained rats with infarction were compared with their sedentary counterparts. Blood flows to the kidneys, organs of the gut, and skeletal muscle during both submaximal and maximal exercise were unaffected by either myocardial infarction or training; no differences between sedentary and trained rats with infarction and sedentary and trained sham-operated rats were found. These results demonstrate that an exercise training program of moderate intensity produces beneficial hemodynamic and metabolic effects in rats with moderate compensated heart failure.
Effects of long-term treatment with amiodarone on exercise hemodynamics and left ventricular relaxation in patients with hypertrophic cardiomyopathy.
Authors: Paulus W J , Nellens P , Heyndrickx G R , Andries E
Published: June 2011

The influence of long-term treatment with amiodarone on exercise hemodynamics and on left ventricular relaxation was studied prospectively in patients with hypertrophic cardiomyopathy. Rest-exercise hemodynamics (n = 9) and echocardiographic relaxation indexes (isovolumic relaxation time, dPW/dt) (n = 11) were measured in control conditions and after 5 weeks of oral amiodarone treatment (600 mg daily first week, 400 mg daily second week, 200 mg daily afterwards). Long-term amiodarone treatment in patients at rest caused a significant drop in heart rate from 80 +/- 11 to 75 +/- 11 beats/min (p less than .05), a rise in mean pulmonary artery pressure from 19 +/- 7 to 25 +/- 10 mm Hg (p less than .02), and a rise in mean pulmonary capillary wedge pressure from 11 +/- 4 to 17 +/- 8 mm Hg (p less than .05). Systemic arterial pressure, cardiac output, and systemic vascular resistance remained unaltered. Exercise tolerance assessed by serial supine bicycle stress testing was reduced in six of nine patients. Amiodarone treatment caused a significant rise in pulmonary capillary wedge pressure from 22 +/- 8 to 37 +/- 9 mm Hg (p less than .001) at the highest identical workloads and from 26 +/- 10 to 37 +/- 9 (p less than .005) at maximal symptom-limited workloads. Similarly, mean pulmonary artery pressure rose from 37 +/- 15 to 51 +/- 18 mm Hg (p less than .01) at highest identical workloads and from 42 +/- 19 to 51 +/- 18 mm Hg (p less than .01) at maximal symptom-limited workloads. There were no significant differences at maximal exercise level in heart rate, systemic arterial pressure, cardiac output, or exercise factor. Echocardiographic studies performed before and during long-term amiodarone treatment revealed no change in isovolumic relaxation time, end-diastolic or end-systolic posterior wall thickness, and peak posterior wall thinning rate. A negative inotropic action of amiodarone could explain the worsened rest and exercise hemodynamics observed during long-term treatment of patients with hypertrophic cardiomyopathy. Echocardiographic relaxation indexes remained unaltered despite the elevated left ventricular filling pressures. This finding could suggest a deleterious effect of amiodarone on myocardial inactivation, possibly similar in mechanism to the depressed myocardial inactivation observed in hypothyroidism.
Early detection of myocardial reperfusion by assay of plasma MM-creatine kinase isoforms in dogs.
Authors: Devries S R , Sobel B E , Abendschein D R
Published: June 2011

To determine whether myocardial reperfusion can be detected promptly by changes in profiles of isoforms of MM-creatine kinase (CK) in plasma, coronary occlusion was induced in 30 conscious dogs and reperfusion was initiated after 1, 2, 3, or 4 hr in 21. The myocardial isoform of MM-CK, MMA, was quantified in serial plasma samples by chromatofocusing. Before coronary occlusion, MMA comprised 13 +/- 7% (SD) of the total CK activity in plasma. The percentage of MMA (MMA%) was elevated before reperfusion, but increased markedly and consistently to a peak of 52 +/- 13% (n = 21) between 30 min and 1 hr after the time of onset of reperfusion. The rate of increase in MMA% was significantly faster with reperfusion at 1 hr (1.44 +/- 0.42% min-1), 2 hr (1.28 +/- 0.45% min-1), or 3 hr (1.02 +/- 0.27% min-1) (p less than .001), but not with reperfusion at 4 hr (0.48 +/- 0.34% min-1) compared with the rate in nonreperfused control dogs (0.29 +/- 0.09% min-1). Furthermore, the rate of increase in MMA% was neither influenced by peak total CK activity (r = -.1) nor dependent on infarct size measured histochemically 24 hr after coronary occlusion (r = -.003). The time from coronary occlusion to the peak of MMA% was reduced by reperfusion at 1 to 3 hr compared with control, but this index was not identified as rapidly as the rate of increase in MMA%. Accordingly, characterization of the rate of increase in MMA% in plasma when reperfusion occurs early after the onset of myocardial infarction permits prompt, reliable, and noninvasive detection of myocardial reperfusion.
Altered spectrum of nitroglycerin action in long-term treatment: nitroglycerin-specific venous tolerance with maintenance of arterial vasodepressor potency.
Authors: Stewart D J , Elsner D , Sommer O , Holtz J , Bassenge E
Published: June 2011

The study of venodilator tolerance to nitroglycerin has been complicated by reflex compensation and by problems in analyzing venous tone in the presence of multiple determinants of venous pressure. We assessed venous tone as total effective vascular compliance (TEVC) under autonomic blockade in six dogs, in the nontolerant state, and during a 5 day infusion of nitroglycerin (1.5 micrograms/kg/min). Under long-term treatment, baseline TEVC was unaffected and the nitroglycerin dose-response relationship for TEVC was shifted to greater than 10-fold higher doses, whereas baseline mean arterial pressure (MAP) was lowered by 17 +/- 3 mm Hg without any shift in nitroglycerin responsiveness. This lowering of MAP was observed only after autonomic blockade. In six additional dogs instrumented with aortic flow probes, nitroglycerin (1.5 micrograms/kg/min) induced a 15 +/- 1% decline in peripheral vascular resistance (PVR) under autonomic blockade, but with reflexes intact these dogs showed no change in PVR and a 21 +/- 10% increase in norepinephrine release rate. We conclude that modest long-term exposure to nitroglycerin results in tolerance to its venodilating effects, whereas arteriolar action is maintained. This tolerance-induced shift in action from venous toward arteriolar dilation is normally masked by compensatory reflexes.
Altered left ventricular diastolic properties during pacing-induced angina in patients with aortic stenosis.
Authors: Fifer M A , Bourdillon P D , Lorell B H
Published: June 2011

An increase in left ventricular diastolic pressure has been repeatedly observed during angina in patients with coronary artery stenoses and regional demand ischemia, but the role of relaxation abnormalities versus left ventricular segmental dyssynchrony is controversial. In contrast, patients with angina due to aortic stenosis are likely to have diffuse rather than segmental ischemia and thus may provide an alternative model for examining the diastolic physiology of angina in man. Accordingly, we examined the hemodynamic manifestations of angina in eight patients with aortic stenosis without significant coronary artery disease. Angina was induced by pacing tachycardia, and hemodynamic and echocardiographic variables were measured in the control period and during angina in the beats immediately after cessation of pacing. Heart rate (control vs angina, 69 +/- 12 vs 70 +/- 11 beats/min, p = NS) and left ventricular peak systolic pressure (207 +/- 39 vs 222 +/- 22 mm Hg, p = NS) were similar in the control and postpacing angina periods. Left ventricular end-diastolic pressure, on the other hand, was significantly higher during postpacing angina (15 +/- 7 vs 28 +/- 8 mm Hg, p less than .01). The time constant of left ventricular pressure decline during isovolumetric relaxation (TL), calculated as the slope of a linear fit of the natural log of pressure vs time, increased from 44 +/- 5 to 51 +/- 7 msec (p less than .05); the time constant TD, derived from the slope of a linear fit of dP/dt vs pressure, also increased slightly, although the change was not statistically significant (69 +/- 5 vs 75 +/- 5 msec, p = .06).(ABSTRACT TRUNCATED AT 250 WORDS)
Time variation of mitral regurgitant flow in patients with dilated cardiomyopathy.
Authors: Keren G , LeJemtel T H , Zelcer A A , Meisner J S , Bier A , Yellin E L
Published: June 2011

Angiographic results in patients with mitral regurgitation suggest that up to 50% of the regurgitant volume occurs during the preejection period. This contrasts markedly with the electromagnetic measurements of mitral regurgitant flow in anesthetized dogs, which suggest that only 5% of mitral regurgitant flow occurs during the preejection period. Therefore, we used two-dimensional and Doppler echocardiography to quantify mitral regurgitation during aortic ejection and in the preejection and postejection periods in eight patients with severe heart failure. Mitral regurgitant volume (RV) was calculated as the difference between total stroke volume (by two-dimensional echocardiography) and forward aortic flow (by pulsed Doppler). Regurgitant velocity (V) and time (RT) were measured by continuous-wave Doppler, and the mean regurgitant area (RAm) was calculated from the RT and mean regurgitant velocity (Vm): RAm = (RV/RT)/Vm. As a first approximation, the RA was assumed to be constant during systole, and the regurgitant volume during aortic ejection and during the preejection and postejection periods was calculated from: RVi = (Vmi) (RTi) (TAm), where Ti represents the duration of the appropriate period. Percentages of total regurgitant volume occurring during the preejection, ejection, and postejection periods were 13 +/- 4%, 79 +/- 5%, and 8 +/- 5%, respectively. Thus, in contrast to previously reported angiographic studies, mitral regurgitation occurs predominantly during the aortic ejection period. These results were not substantially changed by assuming a 20% reduction in effective regurgitant orifice area between the preejection and ejection periods and are consistent with data from chronically instrumented dogs with mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)
Changes in systemic vascular resistance detected by the arterial resistometer: preliminary report of a new method tested during percutaneous transluminal coronary angioplasty.
Authors: Mohr R , Rath S , Meir O , Smolinsky A , Har-Zahav Y , Neufeld H N , Goor D A
Published: June 2011

A recently developed apparatus provides on-line continuous monitoring of systemic vascular resistance (SVR) by means of simple computer analysis of the peripheral arterial waveform. The fundamental equation of this method is Ri = P'/(dP/dt), where dP/dt is the peak dP/dt of the peripheral arterial waveform, P' is the pressure at time of peak dP/dt, and Ri is a resistance index that bears a direct relation to SVR. Eleven patients undergoing percutaneous transluminal coronary angioplasty (PTCA) were studied to evaluate the changes in SVR associated with myocardial ischemia (angina detection). There were 49 balloon inflations, all of which were associated with an increase in Ri (from 38.4 +/- 12 to 81.2 +/- 36 X 10(-3) sec; p less than .01) and a decrease in dP/dt (from 2076 +/- 257 to 1327 +/- 326 mm Hg/sec; p less than .01). In 42 of the balloon inflations these changes were associated with electrocardiographic ST-T changes and in 23 it was also associated with anginal pain. When angina was present, a further increase in Ri (to 97.5 +/- 43 X 10(-3) sec; p less than .01) and a decrease in dP/dt (to 1218 +/- 338 mm Hg/sec; p less than .01) was observed. It was found that myocardial ischemia is associated with an increase in the resistance index and a decrease in dP/dt and can be detected by the resistometer.
Regulation of plasma levels of low-density lipoprotein cholesterol: interpretation of data on low-density lipoprotein turnover in man.
Authors: Meddings J B , Dietschy J M
Published: June 2011

At the present time the most useful technique with which to examine the kinetics of low-density lipoprotein (LDL) cholesterol in vivo is the labeled LDL turnover study. However, a major limitation of this method is that, despite its ability to accurately measure both the plasma LDL concentration and LDL production rate, it cannot directly quantify LDL receptor activity. The present study defines the equations that describe the relationship between LDL cholesterol production rate, LDL receptor number, and plasma LDL cholesterol concentration. These equations provide a method that allows calculation of total LDL receptor activity based on the results of an LDL turnover study. With the use of this technique and data from previously published series, the effects of the genetic absence of receptors, aging, and the treatment of hypercholesterolemia with mevinolin on LDL cholesterol kinetics were analyzed.
Effect of postganglionic vagal stimulation on the organization of atrioventricular nodal conduction in isolated rabbit heart tissue.
Authors: Mazgalev T , Dreifus L S , Michelson E L , Pelleg A
Published: June 2011

Postganglionic stimulation of vagal terminals (PGVS) in the isolated rabbit heart atrioventricular (AV) node was used to study the effects of cholinergic influence on AV nodal conduction. Standard microelectrode techniques were used to record action potentials, predominantly from cells located in the N region of the AV node. In addition, programmed stimulation was used in conjunction with PGVS to initiate or terminate AVN reentry. The introduction of a single short burst of PGVS (total duration 50 to 100 msec, impulse duration 1 msec, and interimpulse interval 6 msec) with subthreshold amplitude for AV node fibers caused reproducible disorganization of the prevailing excitation front. This was manifest as local nonuniform depression of conduction, hump formations in the action potentials, and alteration in the sequence of depolarization. The introduction of repetitive bursts of PGVS revealed a triphasic time course of changes in AV nodal conduction time, representing initial maximal prolongation, relative shortening, and secondary inhibition. It was found that these phases corresponded to vagally induced initial disorganization and a subsequent rebound process. Vagally induced disorganization of the sequence of action potential depolarization was also a triggering mechanism for concealed as well as manifest AV nodal reentry. In the latter case the reentry circuit usually involved the AN region and perinodal atrial tissue. PGVS-induced depression of the N region was also able to block the retrograde wavefront, thereby terminating reentry. The possible relationship of PGVS-induced disorganization of conduction and the inhomogeneous structure of AV node are discussed. The present results provide additional information for better understanding of the AV nodal conduction abnormalities observed clinically and particularly those related to AV node-vagus interaction.
Phasic mitral blood flow and regional left ventricular dimensions: possible mechanism of active assist to ventricular filling.
Authors: Bertha B G , Folts J D
Published: June 2011

Postsystolic myocardial segment shortening (PSS) has been observed in dogs and humans by means of ultrasonic crystals but has never been studied specifically. In this study, both subendocardial and subepicardial regional function in the basal circumflex and midventricular anterior myocardium (LAD) was studied during late systole and early diastole with ultrasonic crystals. Fifteen open-chest dogs were instrumented with electrocardiographic leads; Millar catheters for measurement of left ventricular pressure, left ventricular dP/dt, and aortic blood pressure; flow probes for determination of aortic and mitral blood flow; and subendocardial and subepicardial crystal pairs to measure subendocardial segment length shortening velocity (dL/dt). Crystal pairs were placed in the subendocardial left oblique mode and the extreme subendocardial right oblique mode (-50 and +50 degrees from equator) in the lateral basal (circumflex, n = 9) and anterior midventricular myocardium (LAD, n = 6). Subendocardial segments showed PSS averaging 34 +/- 7% of the total shortening distance in the circumflex bed and 21 +/- 2% in the LAD bed (p = NS). The rate of subendocardial segment shortening during PSS increased 273 +/- 42.6% (p less than .05) relative to the rate of segment shortening during ejection in the circumflex bed and 126 +/- 40% (p less than .05) in the LAD bed (p = NS). The most rapid diastolic increase in subendocardial length (peak +dL/dt) occurred immediately after subendocardial PSS. Subendocardial diastolic peak +dL/dt occurred after the onset of mitral inflow during the acceleration limb of the rapid ventricular filling phase. Overlying subepicardial segments began lengthening 82 +/- 12 msec before onset of subendocardial segment lengthening in the circumflex bed and 63 +/- 9 msec before subendocardial lengthening in the LAD bed (p less than .05), indicating that the subepicardial segment had begun to lengthen while subendocardial segment shortening continued after end-systole. Onset of early segmental subepicardial lengthening varied with respect to the point of end-systole. Early segmental subepicardial lengthening with subendocardial PSS may be a mechanism by which the rapid filling phase of the left ventricle is actively potentiated by storing potential energy released as early diastolic elastic recoil.
Comparison of multiple views for the evaluation of pulmonary arterial blood flow by Doppler echocardiography.
Authors: Lighty G W , Gargiulo A , Kronzon I , Politzer F
Published: June 2011

Forty adult patients underwent Doppler and two-dimensional echocardiographic examination of the pulmonary artery from multiple views to determine the variability in the magnitude of Doppler-determined flow velocity and pulmonary arterial diameter from various echocardiographic windows. Flows were recorded from two or more views in 32 patients (80%). Twelve of these patients (38%) had flow velocities recorded from two or more views that were within 6% of each other. Twenty of these patients (62%) had view-dependent differences in measured flow velocity ranging from 7% to 48%. The commonly used parasternal short-axis view yielded the highest pulmonary arterial flow velocity in only 35% of the patients studied. Determinations of pulmonary arterial blood flow can vary markedly when measured from different sites, and this is presumably due to varying ability to approximate a zero-degree Doppler angle from different views. Measurement of pulmonary arterial flow velocity should be attempted from multiple views, and the highest flow velocity should be selected as that obtained with the best zero-degree Doppler angle approximation.
High-frequency analysis of the surface electrocardiograms of patients with supraventricular tachycardia: accurate identification of atrial activation and determination of the mechanism of tachycardia.
Authors: Kuchar D L , Kelly R P , Thorburn C W
Published: June 2011

Signal processing of the electrocardiogram (ECG) was performed during supraventricular tachycardia (SVT) in 24 patients in an attempt to locate the P wave and to characterize its morphology in three orthogonal planes. In patients with atrioventricular reciprocating tachycardia, a discrete atrial signal could be identified within the ST segment and/or T wave with inferior-to-superior orientation. Atrial activation was identified in patients with primary atrial tachycardia as long as there was a constant relationship between each QRS complex and the preceding atrial signal. Patients with atrioventricular nodal reentrant tachycardia were deduced to have simultaneous atrial and ventricular activation when no atrial signal could be seen elsewhere in the cycle. Mean maximum P wave amplitude was 25.4 +/- 6.3 microV during SVT, with a mean noise level below 1.0 microV. Signal processing of the ECG during SVT enhances the detection of the P wave and the appreciation of P wave morphology, both of which are important factors in the noninvasive determination of the electrophysiologic mechanisms of SVT.
The use of ambulatory monitoring in the prognostic evaluation of patients with sustained ventricular tachycardia treated with amiodarone.
Authors: Veltri E P , Griffith L S , Platia E V , Guarnieri T , Reid P R
Published: June 2011

We recently reported a retrospective experience with serial Holter monitoring as a guide to therapy in patients with sustained ventricular tachycardia treated with amiodarone. To confirm and substantiate these findings, a prospective study was designed that included baseline 24 hr Holter monitoring and serial Holter monitoring after 1 week of therapy with amiodarone. Fifty-two patients with documented sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring were treated with amiodarone. Thirty-four patients (group I) had nonsustained ventricular tachycardia completely suppressed and 18 patients (group II) had continued nonsustained ventricular tachycardia on serial Holter monitoring performed on days 8, 9, and 10 of therapy. At 11.6 +/- 1.0 (mean +/- SE) months follow-up, three (9%) group I patients and 12 (67%) group II patients had recurrent sustained ventricular tachycardia or sudden cardiac death (p less than .01). The sensitivity, specificity, positive and negative predictive value, and predictive accuracy of ventricular tachycardia on 24, 48, and 72 hr Holter monitoring over days 8, 9, and 10 for predicting recurrent sustained ventricular tachycardia or sudden cardiac death were analyzed. The positive and negative predictive values were 89% and 84%, 69% and 89%, and 67% and 91% for 24, 48, and 72 hr Holter monitoring, respectively. Overall predictive accuracy was 85%, 83%, and 83%, respectively. We conclude that early Holter monitoring is useful in assessing the clinical efficacy of amiodarone in patients with sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring.
The renal, forearm, and hormonal responses to standing in the presence and absence of propranolol.
Authors: Bakris G L , Wilson D M , Burnett J C
Published: June 2011

Nine normal volunteers underwent assessment of renal, forearm, and hormonal responses to orthostasis (quiet standing) in the presence and absence of 1 week of oral propranolol (160 mg/day). This was done to test the hypothesis that physiologic decrements in renal function (glomerular filtration rate, effective renal plasma flow, and absolute urinary sodium excretion) are attenuated by propranolol during quiet standing. The present studies, however, demonstrate that propranolol exaggerates the physiologic decrement in glomerular filtration rate, effective renal plasma flow, and absolute urinary sodium excretion during orthostasis. Forearm and renal vascular resistances were also accentuated in the presence of propranolol during quiet standing. These responses were associated with significant increases in plasma norepinephrine. We conclude that long-term administration of propranolol accentuates the physiologic decrement in renal hemodynamic and excretory function as well as in the forearm hemodynamic response to orthostasis in normal subjects.
Arteriovenous carbon dioxide and pH gradients during cardiac arrest.
Authors: Grundler W , Weil M H , Rackow E C
Published: June 2011

In a porcine preparation of cardiac arrest, we demonstrated that there is a marked paradox of venous acidemia and arterial alkalemia. This paradox is related to decreased clearance of CO2 from the lungs when pulmonary blood flow is critically reduced. Accordingly, increased venous PCO2 rather than metabolic acidosis due to lactic acidosis predominates during the initial 8 min of cardiopulmonary resuscitation. Arterial blood gases fail as indicators of systemic acid-base status and therefore as indicators of tissue acidosis.
The effect of vasoactive agents on the left ventricular end-systolic pressure-volume relation in closed-chest dogs.
Authors: Freeman G L , Little W C , O'Rourke R A
Published: June 2011

The left ventricular end-systolic pressure-volume relation has received intense interest as a relatively load-insensitive measure of cardiac performance. In clinical studies, pharmacologic manipulation of blood pressure has been used to determine this relation. Since previous studies have shown that acute changes in the resistance and impedance of the arterial circulation influence the left ventricular end-systolic pressure-volume relation, the use of vasoactive drugs in its determination may affect the results achieved. This study was undertaken to determine whether clinically used vasoactive drugs influence the left ventricular end-systolic pressure-volume relation. Sixteen dogs were previously instrumented with micromanometer pressure transducers and three sets of piezoelectric crystals to permit determination of left ventricular pressure and volume. The dogs were studied after autonomic blockade and sedation. End-systolic pressure-volume relations were generated by caval occlusion at control levels of blood pressure, after infusion of a vasopressor (methoxamine, n = 6; angiotensin II, n = 10), and then after infusion of nitroprusside. A composite end-systolic pressure-volume relation was also constructed with the use of control, vasopressor, and vasodilator points in each dog. Angiotensin II resulted in a leftward shift in the relation (Vo decreased from 14.32 +/- 7.3 to 8.04 +/- 10.4 ml, p less than .05) with no significant effect on slope. Methoxamine shifted the relation to the left (Vo decreased from 13.98 +/- 8.74 to -0.47 +/- 12.06 ml, p less than .05) and also reduced the slope (5.41 +/- 3.09 vs 8.28 +/- 3.94 mm Hg/ml, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
The monophasic action potential upstroke: a means of characterizing local conduction.
Authors: Levine J H , Moore E N , Kadish A H , Guarnieri T , Spear J F
Published: June 2011

The upstrokes of monophasic action potentials (MAPs) recorded with an extracellular pressure electrode were characterized in isolated canine tissue preparations in vitro. The characteristics of the MAP upstroke were compared with those of the local action potential foot as well as with the characteristics of approaching electrical activation during uniform and asynchronous conduction. The upstroke of the MAP was exponential during uniform conduction. The time constant of rise of the MAP upstroke (TMAP) correlated with that of the action potential foot (Tfoot): TMAP + 1.01 Tfoot + 0.50; r2 = .80. Furthermore, changes in Tfoot with alterations in cycle length were associated with similar changes in TMAP: Tfoot = 1.06 TMAP - 0.11; r2 = .78. In addition, TMAP and Tfoot both deviated from exponential during asynchronous activation; the inflections that developed in the MAP upstroke correlated in time with intracellular action potential upstrokes that were asynchronous in onset in these tissues. Finally, the field of view of the MAP was determined and was found to be dependent in part on tissue architecture and the space constant. Specifically, the field of view of the MAP was found to be greater parallel compared with transverse to fiber orientation (6.02 +/- 1.74 vs 3.03 +/- 1.10 mm; p less than .01). These data suggest that the MAP upstroke may be used to define and characterize local electrical activation. The relatively large field of view of the MAP suggests that this technique may be a sensitive means to record focal membrane phenomena in vivo.
Modulated parasystole originating in the sinoatrial node.
Authors: Jalife J , Michaels D C , Langendorf R
Published: June 2011

A computer model of "modulated sinus parasystole" was devised in which two sinus pacemakers interacted electrotonically, entraining each other's periodicity according to their beat-to-beat phasic relationships. Depending on the preestablished rules, the model gave rise to various rhythm patterns that were similar to those recorded in patients with sinoatrial arrhythmias. The validity of the model in predicting clinically observed rhythm disturbances was tested in a case of sinoatrial extrasystolic activity. The sinoatrial origin of parasystolic discharges giving rise to various patterns of group beating in this case was diagnosed according to the following electrocardiographic criteria: premature P waves having contour identical to P waves of basic beats, variable coupling intervals, and absence of compensatory pauses (i.e., returning cycles having duration similar to that of the basic P-P interval). For the analysis, it was assumed that two distinct but closely apposed sinoatrial pacemaker centers were competing for activation of the heart. The model accurately simulated the arrhythmias in the electrocardiographic trace. The best fit was found when the two pacemakers interacted on the basis of "resetting" in one direction and electronic modulation in the other. In fact, under appropriate conditions, the model matched precisely all frequency-dependent patterns of extrasystolic activity observed in the trace. We conclude that the modulated parasystole hypothesis can readily explain the mechanism of sinus extrasystolic discharges whose returning cycle equals the basic P-P interval. Moreover, the model predicts that, when the rules for mutual entrainment between "dominant" and parasystolic sinus pacemaker are appropriate, the returning cycle can be shorter than the basic cycle.
Effects of incremental doses of procainamide on ventricular refractoriness, intraventricular conduction, and induction of ventricular tachycardia.
Authors: Morady F , DiCarlo L A , de Buitleir M , Krol R B , Baerman J M , Kou W H
Published: June 2011

The short-term effects of incremental doses of procainamide (7.5, 15, 22.5, and 30 mg/kg) on right ventricular effective refractory period, intraventricular conduction, and induction of ventricular tachycardia were determined in 31 patients who had a history of sustained, unimorphic ventricular tachycardia. QRS duration during incremental ventricular pacing was used as an index of rate-dependent changes in intraventricular conduction. The mean plasma procainamide concentrations corresponding to the incremental doses were 5.5 +/- 1.2 (+/- SD), 9.0 +/- 1.6, 12.6 +/- 2.2, and 16.3 +/- 3.2 mg/liter. Each incremental dose of procainamide up to a dose of 30 mg/kg resulted in a significant increment in right ventricular effective refractory period and each dose up to 22.5 mg/kg potentiated a rate-dependent prolongation of QRS duration. After the 7.5 mg/kg dose of procainamide, induction of ventricular tachycardia was suppressed in eight of 31 patients. After higher doses of procainamide, induction of ventricular tachycardia was suppressed in two additional patients. In three of 10 patients in whom the induction of ventricular tachycardia was suppressed by 7.5, 15, or 22.5 mg/kg of procainamide, sustained unimorphic ventricular tachycardia was again inducible after a higher dose of procainamide. In three of 31 patients, only nonsustained ventricular tachycardia was inducible after a 7.5 to 22.5 mg/kg dose of procainamide; however, in two of these three patients, sustained ventricular tachycardia was again inducible after administration of a higher dose of procainamide. In conclusion, during electropharmacologic testing with procainamide, it is worthwhile to test a dose of 7.5 mg/kg, because this dose is often effective in patients who respond to this drug. However, the results of this study indicate that procainamide may be effective in suppressing the induction of sustained ventricular tachycardia at a relatively low plasma concentration, but not at a higher plasma concentration. Therefore, during long-term therapy with procainamide it may be important to avoid plasma procainamide concentrations not only lower, but also higher than the concentration that results in the suppression of induction of tachycardia.
Coronary dissection and total coronary occlusion associated with percutaneous transluminal coronary angioplasty: significance of initial angiographic morphology of coronary stenoses.
Authors: Ischinger T , Gruentzig A R , Meier B , Galan K
Published: June 2011

Coronary dissection and total coronary occlusion leading to emergency coronary surgery are the most frequent complications of percutaneous transluminal coronary angioplasty (PTCA) and their occurrence usually is unpredictable. To identify angiographic characteristics of coronary stenoses that may affect the incidence of these complications, the diagnostic pre-PTCA coronary angiograms of 38 consecutive patients (group I) undergoing emergency coronary surgery for dissection or occlusion were reviewed and compared with the angiograms of a random sample of 38 patients (stratified for left anterior descending and right coronary arteries) from a group of 1151 who did not need emergency coronary surgery (group II). Stenosis morphology before angioplasty was considered "complicated" if at least one of the following criteria was present: irregular borders, intraluminal lucency, and localization of stenosis in curve or at bifurcation. Baseline characteristics, maximum inflation pressures, types of balloon catheters used, and routinely registered angiographic stenosis properties (severity, length, eccentricity, and calcification) were similar in both groups. Irregular borders before PTCA were present in 22 of 38 patients in group I vs 10 of 38 in group II (p less than .05), intraluminal lucency in 22 of 38 vs nine of 38 (p less than .05), localization in curve in 27 of 38 pts vs 16 of 38 (p less than .05), and localization at bifurcation in 11 of 38 vs 15 of 38 (NS). Complicated angiographic morphology of coronary stenosis may represent a risk factor for dissection or occlusion. Therefore, although the predictive value of these findings is low, detailed evaluation of angiographic morphology of coronary stenoses may improve patient selection and reduce complication rates of PTCA.
Immediate effect of expiratory loading on left ventricular stroke volume.
Authors: Natarajan T K , Wise R A , Karam M , Permutt S , Wagner H N
Published: June 2011

While the steady-state effects of positive pleural pressure on the circulation have been extensively studied, less is known about the immediate effects of positive intrathoracic pressure on cardiac dynamics. Therefore, we performed electrocardiographically gated radionuclide ventriculography with a respiratory gating technique in nine healthy subjects during quiet breathing and during expiration against a 24 cm H2O expiratory threshold load. During expiration, respiratory loading caused an increase in stroke counts by 29.4% (p less than .001) due to an increase in end-diastolic counts of 26.1% (p less than .001). End-systolic counts also rose 18.8% (p less than .05). The ejection fraction did not change significantly. These findings indicate that the increase in left ventricular stroke volume that occurs during the first 1 or 2 beats of a loaded expiration is due to an increase in left ventricular filling and not to augmentation of left ventricular ejection. This immediate increase in pulmonary venous return may reflect increased distensibility of the left ventricle due to decreased filling of the right ventricle.
Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion.
Authors: Hod H , Lew A S , Keltai M , Cercek B , Geft I L , Shah P K , Ganz W
Published: June 2011

Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second- or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery.(ABSTRACT TRUNCATED AT 250 WORDS)
Selection of patients for cardiac transplantation.
Authors: Copeland J G , Emery R W , Levinson M M , Icenogle T B , Carrier M , Ott R A , Copeland J A , McAleer-Rhenman M J , Nicholson S M
Published: June 2011

Selection of potential cardiac recipients is not a simple process. Identification of patients who are declining from end-stage cardiac disease and may be expected to die within 12 months or less and deciding which of a number of cardiac invalids are reasonable candidates for cardiac transplantation involves prognostication as well as a working knowledge of the expected benefits and survival rates in cardiac transplantation. Screening by means of the currently accepted contraindications for cardiac transplantation is somewhat more difficult in 1986 than it was 10 years ago when these contraindications were changing less rapidly. However, for optimal use of the limited supply of donor organs and maintenance of reasonable survival rates such screening is absolutely necessary. A second area of restriction that is less approachable by the physician is that of financial limitations. It would appear that the working poor and lower middle class may be deprived of the opportunity for cardiac transplantation much as they are deprived of the opportunity for optimal medical care in our society today.
Hemodynamic effects of the beta 1-adrenoceptor partial agonist xamoterol in relation to plasma norepinephrine levels during exercise in patients with left ventricular dysfunction.
Authors: Sato H , Inoue M , Matsuyama T , Ozaki H , Shimazu T , Takeda H , Ishida Y , Kamada T
Published: June 2011

A new cardioselective beta 1-adrenoceptor partial agonist, xamoterol, has been developed for the treatment of heart failure, especially that associated with ischemic heart disease. To investigate the hemodynamic effect of xamoterol in relation to sympathetic nervous activity, hemodynamic variables and plasma norepinephrine (NE) levels were measured at rest and during three graded bicycle exercise tests before and after a single intravenous dose of 0.15 mg/kg xamoterol in 10 patients with mild-to-moderate left ventricular dysfunction. Plasma NE increased with increasing grade of exercise and a linear correlation between plasma NE and heart rate was observed at four time points (at rest and three exercise levels) before and after xamoterol. After administration of xamoterol, the slope of the regression line of plasma NE-heart rate relation was significantly less steep than that before drug. Predose and postdose regression lines crossed at 440 pg/ml of plasma NE. Similar effects were observed on the plasma NE-cardiac index and plasma NE-systolic blood pressure relations (regression lines crossed at 380 and 530 pg/ml of plasma NE, respectively). Thus, xamoterol had a dual agonist-antagonist effect in relation to plasma NE, and the crossover point lay approximately between 400 pg/ml and 500 pg/ml. This level of plasma NE was achieved at a low exercise level and at a heart rate of about 100 beats/min. These results indicate that xamoterol has intrinsic sympathomimetic activity comparable to relatively low sympathetic activity (400 to 500 pg/ml of plasma NE) and therefore acts as a beta 1-agonist when sympathetic nervous activity is below this level and as an antagonist when sympathetic activity is above this level.