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H M Spotnitz

Publications and source records attributed to H M Spotnitz.

At least 55 records · Page 3Linked to original sources
PubMed1994

Time course of perfusion-induced myocardial edema resolution in rats.

Previous studies have demonstrated that crystalloid coronary perfusion can cause myocardial edema, but the time required for resolution of this edema has not been defined. Accordingly, studies were conducted in 30 rats. Myocardial edema was induced by coronary perfusion with 20 cc/kg of Plegisol (294 mOsm/liter) during aortic occlusion, which produced diastolic arrest. This was followed by whole blood reperfusion, which restored normal contractile function. Duration of reperfusion in minutes was zero (group 0, n = 6), one (group 1, n = 6), five (group 5, n = 6), or fifteen (group 15, n = 6). A control group (n = 6) was studied without edema or reperfusion. Data included heart weight and myocardial water content. Left ventricular pressure-volume curves were measured in groups 1, 5, and 15. Myocardial water content increased significantly from 75.7 +/- 0.5% (SD) in the control group to 79.7 +/- 1.1% (P < 0.05) in group 0 and then decreased significantly to 77.3 +/- 0.7, 75.2 +/- 1.4, and 75.3 +/- 1.6% in groups 1, 5, and 15, respectively. Water content in group 1 was also significantly greater than in groups 5 and 15. Heart weight changes were not statistically significant. Normalized pressure-volume relationships shifted rightward with increasing reperfusion time, but changes were not statistically significant. We conclude that edema induced by crystalloid coronary perfusion of the arrested heart resolves in the beating heart after less than 5 min of blood reperfusion.

Animals↗
PubMed1994

Systolic arterial pressure recovery after ventricular fibrillation in pigs.

Ventricular fibrillation (VF) is induced during implantable cardioverter defibrillator insertion and can result in cardiovascular collapse. The relation between repeated VF trials of varying duration and systolic blood pressure (SBP) recovery rate was studied in 6 pigs. Two implantable cardioverter defibrillator patches were placed on the heart, and VF was varied in a cyclic pattern until cardiovascular collapse occurred. A negative logarithmic relation between SBP recovery rate and duration of VF was found in 4 of the pigs with correlation coefficients of 0.62 to 0.97 (p < 0.05). The overall correlation coefficient was 0.51 for all 116 data points (p < 0.001). Although there was a significant (p < 0.05) decrease in average (+/- standard error of the mean) baseline SBP in the second half of each experiment (83 +/- 5 mm Hg versus 77 +/- 6 mm Hg), no significant difference in SBP was observed during VF (17 +/- 1 mm Hg versus 16 +/- 1 mm Hg) or after 15 seconds of SBP recovery (51 +/- 4 mm Hg versus 46 +/- 3 mm Hg) between the two halves of the experiments. Cardiovascular collapse occurred without warning; epinephrine was effective in reversing it. In conclusion, SBP recovery rate and duration of VF have a negative logarithmic relation consistent with a negative effect on left ventricular contractility with prolongation of VF. The onset of cardiovascular collapse during implantable cardioverter defibrillator testing cannot be predicted on the basis of monitored blood pressure alone.

Animals↗
PubMed1994

Systolic arterial pressure recovery after ventricular fibrillation/flutter in humans.

Although the elective induction of cardiac arrest for implantable defibrillator insertion under general anesthesia is widely used, the hemodynamics of recovery of arterial blood pressure after cardiac arrest is not well-defined. Accordingly, the time course of recovery of systolic arterial pressure was studied in seven patients during the repetitive induction of ventricular fibrillation (n = 6) or ventricular flutter (n = 1). The mean number of episodes of cardiac arrest was 7 +/- 2, and the mean drop in systolic pressure was 84 +/- 16 mmHg. The mean recovery time for systolic pressure was 10 +/- 6 seconds, the average systolic pressure recovery rate was 13 +/- 14 mmHg/sec, and the mean percent systolic pressure recovery was 94% +/- 9%. A negative logarithmic relation was found to exist between the rate of systolic arterial pressure recovery and the duration of ventricular fibrillation or flutter with a correlation coefficient of 0.68 to 0.97 (P < 0.05) in five of the seven patients. A linear relation between the time for systolic pressure recovery and duration of asystole was also defined. These results are consistent with the view that prolongation of ventricular fibrillation or flutter increases the duration of arterial pressure recovery through a negative effect on left ventricular contractility. Increased understanding of these relations may lead to increased safety of implantable defibrillator insertion.

Adult↗
PubMed1994

Extrinsic factors influencing left ventricular conductance in situ.

BACKGROUND: The accuracy of conductance measurement of left ventricular (LV) volume is affected by parallel conductance (Vp) from right ventricular (RV) volume as well as surroundings of the heart. No studies have quantified the extrinsic influences on Vp. METHODS AND RESULTS: In six anesthetized pigs, using a median sternotomy and pericardial well, implantable cardioverter defibrillator patches, normal saline, or echocardiography gel were introduced and removed. LV end-diastolic pressure (LVEDP) did not change significantly with these interventions. Raw LV conductance was used to estimate end-diastolic volume (LVEDV), end-systolic volume (LVESV), and stroke volume (SV). Saline significantly increased mean +/- SEM calculated LVEDV from 106 +/- 8 to 131 +/- 6 mL and calculated LVESV from 81 +/- 7 to 110 +/- 5 mL; calculated SV decreased from 25 +/- 3 to 21 +/- 2 mL (P < .05, paired t test). Implantable cardioverter defibrillator patches and gel did not significantly change calculated LV volumes. LV conductance was also measured in arrested hearts during LV filling (5 to 60 mL) at four levels of RV volume (RVV). Using a fixed value for Vp, calculated mean LV volume was 30 +/- 3 mL at RVV = 0, 32 +/- 3 mL at RVV = 20, 33 +/- 3 mL at RVV = 40, and 36 +/- 3 mL at RVV = 60 (P < .01, repeated-measures ANOVA). CONCLUSIONS: While implantable cardioverter defibrillator patches and gel have no statistically significant effect, saline and RVV affect LV volume calculations by conductance, requiring special techniques during cardiopulmonary bypass or caval occlusion.

Animals↗
PubMed1994

Diastolic function in the heterotopic rat heart transplant model. Effects of edema, ischemia, and rejection.

Decreased systolic ventricular function and compliance and increased left ventricular edema and mass have been demonstrated in cardiac allograft rejection. Whether decreased left ventricular compliance in rejection is caused by myocardial edema has not been examined, and compliance in the Ono-Lindsey model has not been reported. Heterotopic rat abdominal cardiac transplantation was performed in ACI isografts (n = 24) and in ACI to Lewis allografts (n = 24). Subgroups were studied on posttransplantation days 0, 1, 3, and 5 (each n = 6). Both transplanted hearts and native hearts were arrested with potassium for the assessment of myocardial water content, heart weight, and the left ventricular pressure-volume relation. In transplanted hearts, myocardial water content did not change in isografts but increased on posttransplantation day 5 in allografts (81.1% on posttransplantation day 5 versus 76.1% on day 0, 77.2% on day 1, and 77.5% on day 3, p < 0.05). Wet and dry heart weight also increased on posttransplantation day 5 in allografts (p < 0.05). The left ventricular pressure-volume relation in transplanted hearts shifted to the left when compared with that in native hearts in all subgroups; these volume differences were statistically significant (p < 0.01) for all pressures above 7.5 mm Hg. This pattern was similar in isografts and allografts on posttransplantation days 0, 1, and 3, and no significant differences between isografts and allografts were demonstrated. On posttransplantation day 5, however, the pressure after a 0.05 ml injection in allografts was greater in transplanted hearts than in native hearts (24 +/- 3 versus 3 +/- 1 mm Hg, p < 0.01). The pressure difference between transplanted and native hearts was also significantly greater in allografts than in isografts (22 +/- 2 versus 6 +/- 1 mm Hg, p < 0.01), indicating an increase in stiffness of allografts. Thus edema and impaired diastolic properties occur concurrently with allograft rejection. Left ventricular volume is abnormal from posttransplantation days 0 to 5 in transplanted hearts but not native hearts in the Ono-Lindsey model with current methods, apparently because of ischemic injury during transplantation.

Animals↗
PubMed1994

Effects of perfusion-induced edema on diastolic stress-strain relations in intact swine papillary muscle.

The mechanism through which edema reduces left ventricular compliance has not been defined. Accordingly, diastolic properties of in situ left ventricular swine papillary muscles were studied in three groups: control (n = 6, 4 degrees to 6 degrees C), edematous (150 mOsm/L coronary perfusion, n = 6, 4 degrees to 6 degrees C), and ischemic contracture (n = 8, 28 degrees C). Lagrangian stress (sigma) and strain (epsilon) were calculated from slow stretch data and approximated by sigma = alpha(e beta epsilon-1). The natural logarithm of stress versus strain was linear over the physiologic range of 0.05 < strain < 0.40. Hypotonic perfusions (1 L x 3) progressively shifted the stress-strain relationship upward and to the left. Compared to baseline, alpha increased significantly (p < 0.05) after perfusion 3 (6.7 +/- 2.1 baseline, 12.2 +/- 6.6 perfusion 1, 12.7 +/- 3.5 perfusion 2, and 42.9 +/- 16.3 gm/cm2 perfusion 3). The constant beta did not change significantly (13.0 +/- 1.5 baseline, 13.1 +/- 1.6 perfusion 1, 13.2 +/- 1.6 perfusion 2, and 14.1 +/- 1.4 perfusion 3). Right ventricular water content increased after each perfusion (77.1% +/- 1.4% baseline, 81.6% +/- 1.3%, 84.7% +/- 1.5%, and 86.9% +/- 1.7%, p < 0.05). With ischemic contracture, alpha increased from 61.9 +/- 17.8 to 173.1 +/- 61.5 gm/cm2 (p > 0.05) and beta increased insignificantly from 6.5 +/- 0.6 to 10.6 +/- 1.8 (p = NS). In the control group all variables were unchanged after 210 minutes. We conclude that myocardial stiffness increases with myocardial edema. This may explain decreased compliance in the edematous left ventricle.

Animals↗
PubMed1993

Prevention of acute regional ischemia with endocardial laser channels.

Laser myocardial revascularization has been shown to reduce mortality and infarct size after left anterior descending coronary artery (LAD) ligation in dogs. It has not been shown to improve myocardial contractility in acute ischemia. In this study a holmium-yttrium-aluminum garnet laser (wavelength, 2.14 microns) was used to create nontransmural myocardial channels from the endocardial surface in the ischemic regions of the canine left ventricle. Twelve mongrel dogs (6 controls, 6 laser myocardial revascularizations) underwent 90 minutes of LAD ligation followed by 6 hours of reperfusion. The ischemic region was determined by methylene blue injection during brief LAD occlusion. Laser myocardial revascularization averaged three channels per square centimeter in the ischemic region created using 12 J/channel (600 mJ/pulse, 10 Hz) before LAD ligation. Contractility was assessed from regional preload recruitable stroke work (RPRSW), using pairs of segment length ultrasonic transducers in the ischemic and the nonischemic regions. Two-dimensional echocardiography corroborated with segmental length findings. In control dogs, the ischemic region was dyskinetic during LAD ligation and reperfusion. Dyskinesis of the ischemic region during systole produced negative values for regional stroke work, and RPRSW was considered zero. In 4 of 6 laser-revascularized dogs, RPRSW remained positive in the ischemic region. Two dogs had intermittent dyskinesis. The difference between laser-revascularized and control dogs in ischemic region RPRSW was significant (p < 0.01 by Fischer's exact test).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1993

Factors confounding impedance catheter volume measurements in vitro.

The impedance catheter allows continuous measurement of ventricular volume. External influences have been described as causing parallel shifts in impedance-measured volumes; however, factors affecting impedance measurements in a nonparallel manner have not been fully characterized. Accordingly, an impedance catheter was placed inside a latex balloon into which known volumes of normal saline solution were injected. Conductive and nonconductive materials were individually placed within the balloon. Impedance was measured with materials touching (T) or not touching (NT) the catheter. Impedance-measured volumes were plotted versus actual volumes. Compared with the line of identity (LID), a statistical difference (p < 0.05) was found in the slopes in the presence of metallic objects only. These included a pacing lead (T, NT) (mT = 1.32m mNT = 1.29 versus mLID = 1.00), titanium (T) (mT = 1.68 versus mLID = 1.00), and aluminum (NT) (mNT = 0.72 versus mLID = 1.00). These changes in slope indicate nonparallel effects on impedance that confound the ability of the impedance catheter to determine volumes in vitro. These observations imply that serial calibration of both the slope constant (alpha) and the intercept (parallel conductance) of impedance may be necessary for in vivo measurements of ventricular volume based on impedance in the presence of metallic objects.

Aluminum↗
PubMed1993

Estimation of myocardial water content using transverse relaxation time from dual spin-echo magnetic resonance imaging.

Dual spin-echo magnetic resonance imaging may be used for calculation of transverse myocardial relaxation time from the signal intensity of the echoes considered. In this study, the ability of myocardial transverse relaxation time (T2) to quantitate myocardial edema of the right ventricle (RV) and left ventricle (LV) was tested. Dual spin-echo magnetic resonance images of the entire hearts were obtained and T2 of the RV and LV myocardium calculated from the signal intensities within multiple regions of interest distributed over the myocardium. Six hearts were intermittently perfused through an aortic cannula with three perfusates of decreasing osmolality. Biopsies were obtained for water content (WC) analysis both before and after imaging the hearts at baseline and post-perfusion. A seventh (control) heart was not perfused; instead dual spin-echo imaging was performed at the same time intervals as in the perfused hearts. Prior to any intervention, there was no significant difference between baseline RV (79.49 +/- 2.10%) and LV (77.99 +/- 2.44%, p = .2) myocardial water content; RV myocardial T2 (59.9 +/- 5.8 msec) was slightly but not significantly longer than that of the LV (54.6 +/- 5.7 msec, p = .1). After induction of edema, strong correlation was found between right ventricular myocardial water content measurements and right ventricular T2 (RV WC = 68.5 + 0.19 x RV T2; N = 27, R = 0.92, p < .0001, SEE = 1.56%). Similarly, strong correlation was found between left ventricular myocardial water content and T2 (LV WC = 62.1 + 0.29 x LV T2; N = 27, R = 0.92, p < .0001, SEE = 1.80%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Does ventricular fibrillation cause myocardial stunning during defibrillator implantation?

Induction of ventricular fibrillation (VF) is an important part of the process of inserting implantable cardioverter defibrillators (ICDs), allowing the measurement of defibrillation thresholds. However, animal studies have revealed that repeated cycles of VF and defibrillation result in depressed left ventricular (LV) function and reduced cardiac output. Short intervals of VF do not affect myocardial contractility but longer periods produce heart failure. Induced VF was used in a canine model to study profound myocardial stunning leading to heart failure, as well as the therapeutic potential of the phosphodiesterase inhibitor, amrinone (combined with epinephrine and norepinephrine). Amrinone was found to significantly (p < 0.05) increase contractility when added to a stable preparation supported by epinephrine and norepinephrine infusion; amrinone or catecholamines alone had no effect. In the clinical setting, the following factors may affect LV contractility during ICD surgery: catecholamines released as a result of hypotension; negative VF; ischemia; antiarrhythmic drugs; anesthetics; and bradycardia after device testing. Patients (n = 125) have tolerated ICD insertion well. Early data reveals no significant changes in ejection fraction. Though rare, death due to myocardial stunning and LV power failure can occur during ICD insertion. It may be possible to use arterial pressure monitoring to predict this event in vulnerable patients.

Animals↗
PubMed1993

Thoracoscopic placement of implantable cardioverter-defibrillator patch leads in sheep.

BACKGROUND: A thoracoscopic technique was developed for the placement of commercially available implantable cardioverter-defibrillator (ICD) patch leads in sheep. METHODS AND RESULTS: Small ICD patch leads (13.5 cm2, A-67) were placed thoracoscopically in sheep (n = 5) that had survived coronary artery ligation from a previous experiment. The technique used three small incisions in the left chest. After lysis of adhesions, the ICD patch lead was introduced through a mediastinoscope. The ICD patch lead was secured in the extrapericardial position with surgical clips placed in the four corners of the ICD patch lead. After 2 weeks, a median sternotomy was performed, and ICD patch leads were reexamined for positioning. Extensive fibrosis was noted to adhere the ICD patch lead to the pericardium. The surgical clips were found intact in all animals without noticeable migration of patch lead position. There was no mortality related to ICD patch lead placement, and estimated blood loss was less than 30 mL without use of cautery. CONCLUSIONS: Commercially available ICD patch leads may be reliably and safely placed with minimal patch migration in sheep using thoracoscopic techniques.

Animals↗
PubMed1993

Quantitative effects of myocardial edema on the left ventricular pressure-volume relation. Influence of cardioplegia osmolarity over two hours of ischemic arrest.

We previously studied edema and left ventricular pressure-volume relations in a porcine heart model in which edema occurred even with hyperosmolar crystalloid cardioplegia. This susceptibility to edema was attributed to venous occlusion and an initial 20-minute period of ischemia. Results did not demonstrate reversal of edema by hyperosmolar perfusates. Accordingly, in the present study, heart weight, myocardial water content, and left ventricular pressure-volume curves were measured before and after perfusion-induced edema in eight isolated, arrested, hypothermic porcine hearts. Cardioplegic solution was infused 2.1 +/- 0.8 minutes after the onset of ischemia, and the atrioventricular ring was not clamped during the administration of cardioplegic solution. Cardioplegic solution (1 L) was infused at intervals of 33 +/- 6 minutes at 4 degrees C. Solution osmolarity was 380 (Stanford solution) or 294 mOsm/L (Plegisol solution). The perfusion sequence was 380-1, 380-2, 294-1, 380-3. Pressure-volume relations were assessed with the use of left ventricular volume at a pressure of 10 mm Hg and the ventricular chamber stiffness constant, beta, derived from P = alpha e beta V. Perfusions 380-1 and 380-2 did not affect the pressure-volume curve. Perfusion 294-1 increased heart weight and water content (p < 0.05) and decreased left ventricular volume at 10 mm Hg compared with perfusions 380-1, 380-2, and 380-3. In addition, beta increased (0.023 +/- 0.005 versus 0.029 +/- 0.006, p < 0.05) after perfusion 294-1, compared with 380-1. Correlation coefficients for linear regressions between left ventricular volume at 10 mm Hg and heart weight and water content were r = 0.84 and r = 0.70, respectively. We conclude that under conditions similar to those used clinically, the left ventricle of the pig does not develop edema with Stanford solution (380 mOsm/L). Edema does follow Plegisol solution (294 mOsm/L) cardioplegia. Edema and reduced compliance are incompletely reversed by hypertonic cardioplegia. The porcine left ventricle can usefully replicate the clinical model.

Animals↗
PubMed1992

Methods of implantable cardioverter-defibrillator-pacemaker insertion to avoid interactions.

Experience with combined transvenous pacemaker and implantable cardioverter-defibrillator insertion in 21 patients is described. Special techniques are needed to avoid potentially lethal pacemaker-implantable cardioverter-defibrillator interaction. Separation between leads for the two devices should be maximized. The electrophysiologic criteria for successful device function can be met, even when some leads for both devices must be placed by a transvenous approach.

Arrhythmias, Cardiac↗
PubMed1992

Computer visualization of left ventricular geometry during the cardiac cycle.

Mathematical expressions regulating ventricular dimensions during the cardiac cycle have been defined. Classical, static images are limited in comparison with ventriculograms, are not intuitive for teaching, and do not effectively convey effects of hypertrophy or dilatation. Accordingly we developed Tachycardia, an interactive menu-driven graphics program. The program allows three-dimensional visualization of the kinetics of the thick-walled, ellipsoidal left ventricle (LV). The user may specify mass, ejection fraction, end-diastolic volume, major to minor axis ratio, and diastole to systole time ratio. Real-time animation of heart rates ranging from 50-150/min is achieved. A library contains animations representing the normal LV, including dilatation and concentric or eccentric hypertrophy. For comparison of differences in LV geometry among ventricles, multiple animations can be viewed simultaneously. We conclude that computerized animation provides an intuitive understanding of the dynamic geometry of the cardiac cycle. User definition of the visualization can provide clinical utility and teaching value.

Computer Graphics↗
PubMed1992

Permanent pacing following cardiac transplantation.

Permanent pacemakers were inserted in 20 of 439 patients who had received 453 orthotopic cardiac allografts since 1980 at the Columbia-Presbyterian Medical Center. Mean age at transplantation was 45 +/- 4 (SEM) years (range 10 to 64). Pacemakers were inserted an average of 2.4 +/- 1 months after transplantation (range 0.4 to 29), 16 of 20 (80%) within the first month. Indications included sinus bradycardia or sinus arrest in 15 (75%), third-degree heart block in 2 (10%), and both sinus node and atrioventricular node dysfunction in 3 (15%). Rejection episodes and pacemaker insertion were associated in 8 patients (40%). Pacing modes included DDD (7 patients, 35%), AAI,R (7 patients, 35%), VVI,R (3 patients, 15%), DDD,R (2 patients, 10%), and VVI (1 patient, 5%). There was no pacing-related morbidity or mortality. Fourteen of 20 patients (70%) are alive and well 3 to 48 months (mean 24 +/- 4) after transplantation. Late follow-up indicated that atrioventricular node dysfunction resolved in one of two patients, sinoatrial node dysfunction improved or resolved in 7/13 patients, and no atrioventricular block developed in 11 (8 to 37 months, mean 22 +/- 3). Permanent pacing can be safely performed following orthotopic cardiac transplantation, predominantly for sinus node dysfunction. The requirement for pacing may reflect ongoing or new onset rejection and patients should therefore be evaluated accordingly. Dual-chamber pacing is probably not necessary unless atrioventricular node dysfunction is coexistent. Further, as most transplant recipients return to an active life-style, AAI,R may be the preferred mode of pacing.

Adolescent↗
PubMed1992

Effects of crystalloid, blood, and University of Wisconsin perfusates on weight, water content, and left ventricular compliance in an edema-prone, isolated porcine heart model.

Coronary perfusion with blood and cardioplegic solutions was examined in isolated, arrested, hypothermic porcine hearts. Myocardial water content, heart weight, and left ventricular diastolic pressure-volume curves were measured before and after coronary perfusion. Statistics were based on exponential curve fitting to pressure-volume data and analysis of variance. Thirty-two pig hearts were divided into five experimental groups and a control group; after control measurements, each experimental group underwent three successive coronary perfusions with 1 L of unmodified blood or a solution of controlled osmolarity, 150 mOsm/L (diluted Plegisol solution), 280 mOsm/L (Plegisol solution and albumin), 334 mOsm/L (University of Wisconsin solution), or 380 mOsm/L (Stanford solution). After each perfusion, measurements were repeated. All experiments were completed within 90 minutes. The first perfusion was delayed 20 minutes after excision of the heart to allow for instrumentation. Each experimental group demonstrated a statistically significant increase in heart weight and myocardial water content and a significant decrease in left ventricular compliance after perfusion. Changes were less pronounced with blood than crystalloids. Edema effects were minimized but not prevented by hyperosmolarity. University of Wisconsin solution appeared unique in minimizing progressive edema after the first perfusion. Over the 81 perfusions studied, changes in left ventricular compliance were linearly related to heart weight and water content. We conclude that in this model, in which edema sensitivity is increased by delayed perfusion and venous occlusion, edema is minimized but not eliminated by whole blood and University of Wisconsin solution. The model appears useful in assessing properties of cardioplegia vehicles intended for use in the injured myocardium.

Adenosine↗