Marc L. Dickstein

The 2013 International Society for Heart and Lung Transplantation Guidelines for mechanical circulatory support: Executive summary

Institutional Affiliations Co-chairs Feldman D: Minneapolis Heart Institute, Minneapolis, Minnesota, Georgia Institute of Technology and Morehouse School of Medicine; Pamboukian SV: University of Alabama at Birmingham, Birmingham, Alabama; Teuteberg JJ: University of Pittsburgh, Pittsburgh, Pennsylvania Task force chairs Birks E: University of Louisville, Louisville, Kentucky; Lietz K: Loyola University, Chicago, Maywood, Illinois; Moore SA: Massachusetts General Hospital, Boston, Massachusetts; Morgan JA: Henry Ford Hospital, Detroit, Michigan Contributing writers Arabia F: Mayo Clinic Arizona, Phoenix, Arizona; Bauman ME: University of Alberta, Alberta, Canada; Buchholz HW: University of Alberta, Stollery Children’s Hospital and Mazankowski Alberta Heart Institute, Edmonton, Alberta, Canada; Deng M: University of California at Los Angeles, Los Angeles, California; Dickstein ML: Columbia University, New York, New York; El-Banayosy A: Penn State Milton S. Hershey Medical Center, Hershey, Pennsylvania; Elliot T: Inova Fairfax, Falls Church, Virginia; Goldstein DJ: Montefiore Medical Center, New York, New York; Grady KL: Northwestern University, Chicago, Illinois; Jones K: Alfred Hospital, Melbourne, Australia; Hryniewicz K: Minneapolis Heart Institute, Minneapolis, Minnesota; John R: University of Minnesota, Minneapolis, Minnesota; Kaan A: St. Paul’s Hospital, Vancouver, British Columbia, Canada; Kusne S: Mayo Clinic Arizona, Phoenix, Arizona; Loebe M: Methodist Hospital, Houston, Texas; Massicotte P: University of Alberta, Stollery Children’s Hospital, Edmonton, Alberta, Canada; Moazami N: Minneapolis Heart Institute, Minneapolis, Minnesota; Mohacsi P: University Hospital, Bern, Switzerland; Mooney M: Sentara Norfolk, Virginia Beach, Virginia; Nelson T: Mayo Clinic Arizona, Phoenix, Arizona; Pagani F: University of Michigan, Ann Arbor, Michigan; Perry W: Integris Baptist Health Care, Oklahoma City, Oklahoma; Potapov EV: Deutsches Herzzentrum Berlin, Berlin, Germany; Rame JE: University of Pennsylvania, Philadelphia, Pennsylvania; Russell SD: Johns Hopkins, Baltimore, Maryland; Sorensen EN: University of Maryland, Baltimore, Maryland; Sun B: Minneapolis Heart Institute, Minneapolis, Minnesota; Strueber M: Hannover Medical School, Hanover, Germany Independent reviewers Mangi AA: Yale University School of Medicine, New Haven, Connecticut; Petty MG: University of Minnesota Medical Center, Fairview, Minneapolis, Minnesota; Rogers J: Duke University Medical Center, Durham, North Carolina

Heart reduction surgery: an analysis of the impact on cardiac function.

OBJECTIVES Reports of improved ejection fraction, coupled with decreased filling pressures, have prompted a number of centers to begin evaluating the efficacy of heart reduction surgery to ameliorate symptoms of heart failure. However, the impact of this operation on cardiac mechanics is unknown. We applied a multiple compartment elastance model to simulate the effects of excising cardiac mass on heart function. METHODS The left ventricle was divided into two functional compartments to simulate excision of part of the wall. At multiple increments of mass reduction, the resulting end-systolic elastance, ejection fraction, stroke volume, end-diastolic pressure and volume, and diastolic stiffness were determined. RESULTS Changes in systolic function were accompanied by offsetting changes in diastolic function; consequently, overall pump function (the Frank-Starling Relationship) was found to be depressed. The geometric rearrangement associated with this operation leads to a reduction in wall stress for a given level of pressure generation, thus implying an increase in the efficiency with which wall stress is transduced into intraventricular pressure. CONCLUSIONS Overall pump function is depressed in the short run after heart reduction surgery. However, on the basis of theoretic arguments, heart reduction surgery may have long-term beneficial implications. Importantly, this analysis revealed that changes in parameters of ventricular function have different implications during heart reduction surgery than when such changes are observed with inotropism caused by acute pharmacologic therapy.

Assessment of right ventricular contractile state with the conductance catheter technique in the pig

OBJECTIVE Since the conductance catheter method has facilitated evaluation of left ventricular contractile state in both laboratory and clinical studies, the aim of this study was to determine whether the technique is similarly useful for the right ventricle. METHODS A series of right ventricular pressure-volume loops was obtained in seven open chest pigs during transient vena caval occlusion using a 12-electrode conductance catheter. End systolic pressure-volume relationships, stroke work-end diastolic volume relationships, and dP/dt-end diastolic volume relationships were compared at control and during infusion of dobutamine and esmolol. RESULTS Right ventricular pressure-volume loops generated with the conductance catheter were of a shape consistent with those previously reported by other volume measurement techniques, and responded to changes in inotropic state in a predictable fashion. Dobutamine shifted the three contractile relationships leftward, whereas esmolol shifted them rightward. Comparisons of stroke volume derived with the conductance catheter and with a pulmonary artery flow probe demonstrated the ability of the conductance technique to measure relative volume changes. CONCLUSIONS The conductance catheter provides a continuous measure of right ventricular volume that was used to detect changes in right ventricular contractile state in pigs. This represents a promising and much needed method for the evaluation of right ventricular function.

Validation Study of a New Transit Time Ultrasonic Flow Probe for Continuous Great Vessel Measurements

Continuous measurement of cardiac output is important during experimental and clinical cardiac surgery as an indicator of ventricular function. Previous flow probes underestimated flow secondary to position and flow (S-series probes; Transonic Systems, Inc., Ithaca, NY), required frequent calibrations (electromagnetic), and were cumbersome to use. The new A-series probe (ASP) by Transonic Systems, Inc., uses a new X method of ultrasonic illumination insensitive to perturbations in flow. The ASPs were found to be accurate during in vitro studies, but have not been validated in vivo. Six anesthetized pigs were instrumented for right atrium to left atrium bypass, and ASPs were placed on the ascending aorta and pulmonary artery. Baseline measurements included aortic (Ao) and pulmonic flow (P), and thermodilution (Td) cardiac output. Animals then were placed on right heart bypass, and flow was randomly varied from 1 to 6 L/min, and Ao flow was recorded. In addition, ASPs were rotated and their direction reversed. After data collection, the occlusive roller pump (RP) was calibrated using a timed collection method. Calibrated RP flows were plotted versus ASP flows, and regression was applied. There was no difference between mean Ao, P, and Td cardiac outputs at baseline. In addition, changes in position and direction of the probe did not affect measurement of flow. The ASPs showed a highly linear correlation with RP ([r = 0.98, p < 0.01] ASP[L/min] = 0.98 RP-0.032). During laminar flow states, ASPs are accurate and insensitive to position on the great vessels.

A computational method of prediction of the end- diastolic pressure-volume relationship by single beat

The end-diastolic pressure–volume relation (EDPVR) is an important descriptor of passive cardiac pump properties. However, clinical utility has been limited by the need for measurement of pressures and volumes over relatively large ranges. In this protocol, we describe an algorithm to estimate the entire EDPVR in humans from a single measured pressure–volume (P–V) point. This algorithm was developed from observations made from accurately measured EDPVRs of human hearts, which indicated that when normalized by appropriate left ventricular volume scaling (to arrive at volume-normalized EDPVRs, EDPVRn) EDPVRns were nearly identical in all patients. In this protocol, we demonstrate how to use EDPVRns to predict a second P–V point on the EDPVR, in which case the entire EDPVR can then be predicted. With recent advances for accurate noninvasive measurement of end-diastolic pressure and volumes, this protocol permits the assessment of passive properties in a broader range of research and clinical settings.

Electric currents applied during the refractory period can modulate cardiac contractility in vitro and in vivo.

Daniel Burkhoff MD PhD , Itzik Shemer , Bella Felzen , Juichiro Shimizu , Yuval Mika , Marc Dickstein , David Prutchi , Nissim Darvish 3 and Shlomo A. Ben-Haim 2,5 Divisions of Circulatory Physiology and Cardiology, Cardiac Physiology Laboratory, Department of Medicine, Columbia University, N.Y., Impulse Dynamics, Tirat HaCarmel 39120, Israel, Department of Physiology and Biophysics, The Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, P.O.B. 9649, Haifa 31096, Israel, Department of Anesthesiology, Columbia University, N.Y., Harvard-Thorndike Arrhythmia Institute, Beth-Israel Hospital, 330 Brookline Ave, Boston, Massachusetts 02215, USA

Iatrogenic Myocardial Edema: Increased Diastolic Compliance and Time Course of Resolution in Vivo

BACKGROUND Perfusion-induced edema reduces diastolic compliance in isolated hearts, but this effect and the time for edema to resolve after blood reperfusion have not been defined in large animals. METHODS Edema was induced by coronary perfusion with Plegisol (750 mL, 289 mOsm/L) during a 1-minute aortic occlusion in 6 pigs. This was followed by whole blood reperfusion, inotropic support, and circulatory assistance until sinus rhythm and contractile function were restored. A control group (n = 6) was treated similarly, with 1 minute of electrically induced ventricular fibrillation and no coronary perfusion. Recorded data included electrocardiogram, left ventricular pressure and conductance, aortic flow, and two-dimensional echocardiography. Preload reduction by vena caval occlusion was used to define systolic and diastolic properties. Data were recorded at baseline and at 15-minute intervals for 90 minutes after reperfusion. RESULTS In the edema group, average left ventricular mass (132 +/- 7 [standard error of the mean] versus 106 +/- 4 g) and ventricular stiffness constant (0.15 +/- 0.02 versus 0.05 +/- 0.01) increased after Plegisol versus baseline (p < 0.05), returning to normal after 45 minutes of reperfusion. In controls, mass (118 +/- 6 versus 116 +/- 4 g) and ventricular stiffness (0.06 +/- 0.01 versus 0.05 +/- 0.01) did not change significantly. There was no significant change in systolic function. Myocardial water content at the end of the study was not different for the two groups. CONCLUSIONS Crystalloid-induced edema and diastolic stiffness resolve after 45 minutes in pigs. This suggests that edema caused solely by cardioplegia during cardiac operations should not cause significant perioperative ventricular dysfunction.

The detection of peripheral venous pulsation using the pulse oximeter as a plethysmograph

The pulse oximeter can serve as a sensitive photoelectric plethysmograph in the operating room. It was noted in several cases that the plethysmographic waveform showed a high degree of variability during diastole. Three patients are described with discrete diastolic peaks on the plethysmograph. Further investigation revealed that these diastolic peaks appear to correlate with peripheral venous pulsation, which seems to have a central venous origin. Evidence is presented that the plethysmographic detection of the venous pulse may be useful in estimating the changing volume status of the patient.

Disparity of isoflurane effects on left and right ventricular afterload and hydraulic power generation in swine

The interaction between myocardial and vascular effects of anesthetics has a potential impact on how these drugs influence performance of the heart.Most studies have focused on volatile anesthetic effects on the left ventricle (LV) and systemic circulation. Whether the right ventricle (RV) and pulmonary circulation respond in a similar fashion, however, is unclear. In the present study, we therefore examined the dose-related effects of isoflurane on LV and RV contractility and total afterload and related changes to simultaneous effects on the hydraulic power generated by each chamber. Two groups of swine were studied: one received no additional treatment before isoflurane (ISO, n = 6), and the other received hexamethonium, atropine, and propranolol to produce autonomic blockade before isoflurane administration (ISO+AB, n = 4). For each experiment, measurements were made of RV and LV regional segment lengths and pressures, along with proximal aortic and pulmonary arterial (PA) blood flow and pressure during the administration of 0, 0.5, 1.0, and 1.5 minimum alveolar anesthetic concentration (MAC) isoflurane. Contractility was assessed by calculating the regional preload recruitable stroke work slope (PRSW). Afterload was characterized in both nonpulsatile and pulsatile terms by calculating aortic input impedance magnitude (Z). From these data, total arterial resistance (R), characteristic impedance (Z (C)), and vascular compliance (C) were determined with reference to a three-element Windkessel model of the circulation. Additionally, steady-state (WSS), oscillatory (WOS), and total (WT) hydraulic power output of each ventricle was calculated. In the ISO group, isoflurane produced a nearly threefold greater decrease of peak systolic pressure in the LV than in the RV, yet the dose-related decrease of regional PRSW was virtually the same in both chambers. In the aorta, isoflurane produced a maximal 25% reduction in R at 1.0 MAC and doubled C without a significant change in ZC. Alternatively, PA R was increased from baseline at 1.0 and 1.5 MAC, whereas ZC was increased from all other values at 1.5 MAC. PA C was not altered by isoflurane. In ISO+AB pigs, PA ZC at baseline was higher than that evident in ISO animals but was not altered by isoflurane. In contrast, baseline aortic R was lower in ISO+AB pigs but was still modestly reduced by 1.0 MAC isoflurane. In ISO animals, WT and WSS from both ventricles demonstrated dose-related decreases, but the reductions in LV WT and WSS were greater than those for the RV at all doses. Accordingly, the power requirement per unit flow decreased for the LV but remained constant for the RV. WOS for both ventricles was also reduced by isoflurane. However, the LV WOS to WT ratio increased, which indicates that more power was lost to the system by pulsation. In contrast, reductions in RV WT and W (OS) were nearly parallel at all isoflurane doses, and the WOS to WT ratio was unchanged. In the ISO+AB group, isoflurane-induced alterations in LV and RV power characteristics were similar to those in the ISO group. These data indicate that, despite similar effects on biventricular contractility, isoflurane exerts qualitatively different effects on RV and LV afterload, in part via alteration in autonomic nervous activity, that influence the distribution of power output between steady-state and pulsatile components. Implications: In this study, we examined the effects of isoflurane on cardiac performance in swine and found that, although the drug depresses contraction of both the left and right ventricles similarly, it has different effects on forces that oppose the ejection of blood. These findings demonstrate that the two interdependent pumps that comprise the heart can be influenced differently by anesthetic drugs. (Anesth Analg 1998;87:511-21)

Inhaled Nitric Oxide Is Not A Myocardial Depressant In A Porcine Model Of Heart Failure

BACKGROUND Inhaled nitric oxide has been shown to be a potent and selective pulmonary vasodilator. Reports of increases in left ventricular end-diastolic pressure and episodes of pulmonary edema during the clinical use of inhaled nitric oxide in patients with preexisting left ventricular dysfunction have raised concerns that this agent may have myocardial depressant effects. We therefore undertook a study of the effects of inhaled nitric oxide on myocardial contractility in a porcine model of ventricular failure and pulmonary hypertension. METHODS After inducing heart failure in 10 pigs by rapid ventricular pacing, hemodynamic measurements and pressure-volume diagrams (by the conductance method) were obtained in six animals at baseline and during administration of inhaled nitric oxide at concentrations of 20 and 40 ppm. Myocardial contractile state was assessed by the end-systolic pressure-volume relationship and preload-recruitable stroke work, whereas diastolic function was measured in terms of the end-diastolic pressure-volume relationship and the pressure decay time constant T. RESULTS Baseline hemodynamics reflected heart failure and pulmonary hypertension, and inhaled nitric oxide induced significant reductions in mean pulmonary artery pressure and pulmonary vascular resistance. Although left ventricular end-diastolic pressure increased during administration of inhaled nitric oxide, no changes were observed in measures of systolic or diastolic function. CONCLUSIONS Inhaled nitric oxide reduced pulmonary vascular resistance but did not alter myocardial contractility or diastolic function. Increases in left ventricular end-diastolic pressure during inhaled nitric oxide therapy are therefore not due to myocardial depression and may be related to increases in volume delivery to the left side of the heart resulting from reduced pulmonary vascular resistance.