Measurement Of Left Ventricular Pressure Research Articles

Measuring Left Ventricular Pressure in Late Embryonic and Neonatal Mice

Blood pressure increases significantly during embryonic and postnatal development in vertebrate animals. In the mouse, blood flow is first detectable around embryonic day (E) 8.5(1). Systolic left ventricular (LV) pressure is 2 mmHg at E9.5 and 11 mmHg at E14.5(2). At these mid-embryonic stages, the LV is clearly visible through the chest wall for invasive pressure measurements because the ribs and skin are not fully developed. Between E14.5 and birth (approximately E21) imaging methods must be used to view the LV. After birth, mean arterial pressure increases from 30 - 70 mmHg from postnatal day (P) 2 - 35(3). Beyond P20, arterial pressure can be measured with solid-state catheters (i.e. Millar or Scisense). Before P20, these catheters are too big for developing mouse arteries and arterial pressure must be measured with custom pulled plastic catheters attached to fluid-filled pressure transducers(3) or glass micropipettes attached to servo null pressure transducers(4). Our recent work has shown that the greatest increase in blood pressure occurs during the late embryonic to early postnatal period in mice(5-7). This large increase in blood pressure may influence smooth muscle cell (SMC) phenotype in developing arteries and trigger important mechanotransduction events. In human disease, where the mechanical properties of developing arteries are compromised by defects in extracellular matrix proteins (i.e. Marfan's Syndrome(8) and Supravalvular Aortic Stenosis(9)) the rapid changes in blood pressure during this period may contribute to disease phenotype and severity through alterations in mechanotransduction signals. Therefore, it is important to be able to measure blood pressure changes during late embryonic and neonatal periods in mouse models of human disease. We describe a method for measuring LV pressure in late embryonic (E18) and early postnatal (P1 - 20) mice. A needle attached to a fluid-filled pressure transducer is inserted into the LV under ultrasound guidance. Care is taken to maintain normal cardiac function during the experimental protocol, especially for the embryonic mice. Representative data are presented and limitations of the protocol are discussed.

Transauricular embolization of the rabbit coronary artery for experimental myocardial infarction: comparison of a minimally invasive closed-chest model with open-chest surgery

IntroductionTo date, most animal studies of myocardial ischemia have used open-chest models with direct surgical coronary artery ligation. We aimed to develop a novel, percutaneous, minimally-invasive, closed-chest model of experimental myocardial infarction (EMI) in the New Zealand White rabbit and compare it with the standard open-chest surgical model in order to minimize local and systemic side-effects of major surgery.MethodsNew Zealand White rabbits were handled in conformity with the "Guide for the Care and Use of Laboratory Animals" and underwent EMI under intravenous anesthesia. Group A underwent EMI with an open-chest method involving surgical tracheostomy, a mini median sternotomy incision and left anterior descending (LAD) coronary artery ligation with a plain suture, whereas Group B underwent EMI with a closed-chest method involving fluoroscopy-guided percutaneous transauricular intra-arterial access, superselective LAD catheterization and distal coronary embolization with a micro-coil. Electrocardiography (ECG), cardiac enzymes and transcatheter left ventricular end-diastolic pressure (LVEDP) measurements were recorded. Surviving animals were euthanized after 4 weeks and the hearts were harvested for Hematoxylin-eosin and Masson-trichrome staining.ResultsIn total, 38 subjects underwent EMI with a surgical (n = 17) or endovascular (n = 21) approach. ST-segment elevation (1.90 ± 0.71 mm) occurred sharply after surgical LAD ligation compared to progressive ST elevation (2.01 ± 0.84 mm;p = 0.68) within 15-20 min after LAD micro-coil embolization. Increase of troponin and other cardiac enzymes, abnormal ischemic Q waves and LVEDP changes were recorded in both groups without any significant differences (p > 0.05). Infarct area was similar in both models (0.86 ± 0.35 cm in the surgical group vs. 0.92 ± 0.54 cm in the percutaneous group;p = 0.68).ConclusionThe proposed model of transauricular coronary coil embolization avoids thoracotomy and major surgery and may be an equally reliable and reproducible platform for the experimental study of myocardial ischemia.

Prognostic Utility of Left Ventricular End-Diastolic Pressure in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Measurement of left ventricular end-diastolic pressure (LVEDP) is readily obtainable in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). However, the prognostic utility of LVEDP during primary PCI has never been studied. LVEDP was measured in 2,797 patients during primary PCI in the Harmonizing Outcomes with RevascularIZatiON and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial. Outcomes were assessed at 30 days and 2 years stratified by medians of LVEDP. Multivariable analysis was performed to determine whether LVEDP was an independent determinate of adverse outcomes. The median (interquartile range) for LVEDP was 18 mm Hg (12 to 24). For patients with LVEDP >18 mm Hg versus those with ≤18 mm Hg, hazard ratios (95% confidence intervals) for death and death or reinfarction at 30 days were 2.00 (1.20 to 3.33, p = 0.007) and 1.84 (1.24 to 2.73, p = 0.002), respectively, and at 2 years were 1.57 (1.12 to 2.21, p = 0.009) and 1.45 (1.14 to 1.85, p = 0.002), respectively. Patients in the highest quartile of LVEDP (≥24 mm Hg) were at the greatest risk of mortality. Only a weak correlation was present between LVEDP and left ventricular ejection fraction (LVEF; R(2) = 0.03, p <0.01). By multivariable analysis increased LVEDP was an independent predictor of death or reinfarction at 2 years (hazard ratio 1.20, 95% confidence interval 1.02 to 1.42, p = 0.03) even after adjustment for baseline LVEF. In conclusion, baseline increased LVEDP is an independent predictor of adverse outcomes in patients with STEMI undergoing primary PCI even after adjustment for baseline LVEF. Patients with LVEDP ≥24 mm Hg are at the greatest risk for early and late mortality.

Effects of mechanical limitation of apical rotation on left ventricular relaxation and end-diastolic pressure

Left ventricular (LV) twist is thought to play an important role in cardiac function. However, how twist affects systolic or diastolic function is not understood in detail. We acquired apical and basal short-axis images of dogs undergoing open-chest procedures (n = 15) using a GE Vivid 7 at baseline and during the use of an apical suction device (Starfish) to limit apical rotation. We measured LV pressure and stroke volume using a micromanometer-tipped catheter and an ultrasonic flow probe, respectively. Peak radial strain, peak rotation, peak twist, peak systolic twisting rate (TR), peak untwisting rate during isovolumic relaxation period (UR(IVR)), and peak early diastolic untwisting rate after mitral valve opening (UR(E)) were determined using speckle tracking echocardiography. Immobilizing the apex with gentle suction significantly decreased apical rotation (-50 ± 27%) and slightly increased basal rotation, resulting in a significant decrease in twist. The time constant of LV relaxation (τ) was prolonged, and LV end-diastolic pressure increased. TR and UR(IVR) decreased. LV systolic pressure, peak positive and negative first derivative of LV pressure (±dP/dt), stroke volume, radial strain, and UR(E) were not changed. The correlation between τ and UR(IVR) (r = 0.63, P = 0.0006) was stronger than that between peak +dP/dt and TR (r = 0.46, P = 0.01). Diastolic function was impaired with reduced apical rotation and UR(IVR) when the apex of the heart was immobilized using an apical suction device.

A tale of two pressures: A case of pseudo‐prosthetic mitral valve stenosis

We present a case of an 83-year-old female with past medical history of rheumatic fever associated mitral stenosis for which she underwent mitral commissurotomy 25 years prior to presentation. Subsequently, she underwent coronary artery bypass grafting and mitral valve replacement with a bio-prosthetic valve 8 years prior to presentation. Presently, she started experiencing worsening dyspnea and heart failure symptoms. Echocardiography showed mildly reduced left ventricular ejection fraction with severe aortic stenosis and pulmonary hypertension. The bioprosthetic mitral valve was functioning normally. We performed right and left heart catheterization for evaluation. Peak aortic gradient was 50 mm Hg with a mean gradient of 39 mm Hg. Aortic valve area was calculated to be 0.31 cm(2). However, simultaneous measurement of left ventricular and wedge pressures showed a significant gradient of 11 mm Hg across the mitral valve with a calculated mitral valve area of 0.4 cm(2). Because of discordant information between echocardiographic and hemodynamic data, we proceeded with trans-septal puncture to directly measure left atrial pressures. Simultaneous left atrial and left ventricular pressure measurement demonstrated a mean gradient of 4 mm Hg across the mitral valve with an area calculated at 1.9 cm(2). We review the tracings in detail and discuss the pitfalls of using pulmonary capillary wedge pressure as a surrogate for left atrial pressure.

Simultaneous measurement of arterial and left ventricular pressure in conscious, freely moving rats by telemetry

Simultaneous measurement of arterial and left ventricular pressure in conscious, freely moving rats by telemetry

Left ventricular pressure (LVP) measurements in anesthetized guinea-pigs: Method validation and comparison with the QA interval

Left ventricular pressure (LVP) measurements in anesthetized guinea-pigs: Method validation and comparison with the QA interval

Left ventricular pressure (LVP) measurement in conscious small animals via a novel solid state telemetry pressure sensor

Left ventricular pressure (LVP) measurement in conscious small animals via a novel solid state telemetry pressure sensor

Association between cardiopulmonary exercise and dobutamine stress testing in ambulatory patients with idiopathic dilated cardiomyopathy: A comparison with peak VO2 and VE/VCO2 slope

BackgroundBoth peak VO2 and VE/VCO2 slope are considered to be useful predictors of cardiovascular events. The left ventricular (LV) response to dobutamine stress testing (DST) also provides useful prognostic information. However, the relationship between these variables has not been fully investigated. Therefore, the aim of this study is to investigate the association between myocardial contractile reserve measured by DST and cardiopulmonary exercise testing (CPX) variables in patients with idiopathic dilated cardiomyopathy (IDCM). MethodsThirty-eight patients were subjected to CPX as well as cardiac catheterization for measurement of LV pressure. The maximum first derivative of LV pressure (LV dP/dtmax) was measured at baseline and during dobutamine infusion at incremental doses of 5, 10, and 15μgkg−1min−1. LV dP/dtmax at baseline and the percentage increase in LV dP/dtmax (ΔLV dP/dtmax) induced by DST served as indices of LV contractility and myocardial contractile reserve, respectively. ResultsPeak VO2, and VE/VCO2 slope were 18.6mLkg−1min−1 and 32.3, respectively. Peak VO2 was not correlated with LV dP/dtmax at baseline. However, peak VO2 was significantly correlated with ΔLV dP/dtmax, and the correlation became more pronounced as the dose of dobutamine was increased. There was no correlation between VE/VCO2 slope and ΔLV dP/dtmax. Multivariate regression analysis revealed that ΔLV dP/dtmax was independently correlated with peak VO2 (p=0.011). ConclusionsPeak VO2, but not VE/VCO2 slope, may reflect myocardial contractile reserve in ambulatory patients with IDCM. This study population is small, and therefore large confirmatory studies are needed.

Variability of Left Ventricular Outflow Tract Gradient During Cardiac Catheterization in Patients With Hypertrophic Cardiomyopathy

This study characterizes left ventricular outflow tract (LVOT) gradient variability in patients with hypertrophic cardiomyopathy (HCM) during cardiac catheterization. Management of HCM is directed by the presence and magnitude of LVOT obstruction. The magnitude and clinical impact of spontaneous variability during a single cardiac catheterization has not been described. Fifty symptomatic patients with HCM (mean age 55 ± 15 years; 48% men) underwent cardiac catheterization with high-fidelity, micromanometer-tip catheters and transseptal measurement of left ventricular pressures. Obstruction was defined as resting LVOT gradient ≥ 30 mm Hg and severe obstruction as ≥ 50 mm Hg. Variability in LVOT gradient was calculated as the difference of the largest and smallest LVOT gradients in the absence of provocative maneuvers or interventions. The largest LVOT gradient was 54.6 ± 56.4 mm Hg. The spontaneous variability in LVOT gradient was 49.0 ± 53.1 mm Hg (range 0 to 210.8 mm Hg, median 15 mm Hg). Discrepant classification of resting LVOT gradient severity was possible in 25 patients (50%). Twenty patients (40%) with severe obstruction could have been misclassified with regard to obstruction severity. In patients with HCM, the LVOT gradient fluctuates significantly during a single hemodynamic assessment. Spontaneous variability could lead to misclassification of obstruction severity in one-half of studied patients. The dynamic nature of LVOT obstruction must be considered when assessing resting hemodynamics or the success of a given intervention during cardiac catheterization.

88 Evaluation of the impact of AV delay variation on the acute mechanoenergetic efficiency of cardiac resynchronisation therapy and assessment of performance of non-invasive vs invasive haemodynamic optimisation

BackgroundThe impact of varying AV delay on the acute mechanoenergetic efficiency of cardiac resynchronisation therapy (CRT) is not known; nor is known if non-invasive haemodynamic optimisation by blood pressure agrees...

A bio-telemetric device for measurement of left ventricular pressure–volume loops using the admittance technique in conscious, ambulatory rats

This paper presents the design, construction and testing of a device to measure pressure–volume loops in the left ventricle of conscious, ambulatory rats. Pressure is measured with a standard sensor, but volume is derived from data collected from a tetrapolar electrode catheter using a novel admittance technique. There are two main advantages of the admittance technique to measure volume. First, the contribution from the adjacent muscle can be instantaneously removed. Second, the admittance technique incorporates the nonlinear relationship between the electric field generated by the catheter and the blood volume. A low power instrument weighing 27 g was designed, which takes pressure–volume loops every 2 min and runs for 24 h. Pressure–volume data are transmitted wirelessly to a base station. The device was first validated on 13 rats with an acute preparation with 2D echocardiography used to measure true volume. From an accuracy standpoint, the admittance technique is superior to both the conductance technique calibrated with hypertonic saline injections, and calibrated with cuvettes. The device was then tested on six rats with 24 h chronic preparation. Stability of animal preparation and careful calibration are important factors affecting the success of the device.

Left ventricular pressure measurement in conscious rats via telemetry

The development of a new telemetry device with a solid state micro-tip 2 Fr sensor has opened up the possibility of recording left ventricular pressure (LVP) chronically in the conscious rat. With particular relevance to LVP measurement is the possibility that high frequency sampling at 2000 Hz permits accurate determination of dP/dT. In the present study, we have explored the surgical placement and long-term stability of the sensor for LVP measurement. We implanted the body of the TRM54P transmitter in the abdomen of rats and used a transdiaphragmatic approach to implant the tip of the catheter through the apex of the left ventricle. The rats were then monitored for 4 to 6 weeks after surgery. To assess the effect of chronic catheter placement, echocardiography was used both before and three weeks after implantation to determine fractional shortening. Our ability to measure changes in dP/dT was assessed using subcutaneous injections of verapamil, isoproterenol and propranolol. Maximum dP/dT values in conscious rats were between 9,000 mmHg/s and 14,000 mmHg/s on the third day after surgery (average 11,000 mmHg/s) and were subsequently stable for at least 4 weeks. The results of this study show that we can accurately measure LVP over long periods in the conscious rat without inducing significant impairment of cardiac function.

Usefulness of Soluble Endoglin as a Noninvasive Measure of Left Ventricular Filling Pressure in Heart Failure

Usefulness of Soluble Endoglin as a Noninvasive Measure of Left Ventricular Filling Pressure in Heart Failure

Usefulness of Soluble Endoglin as a Noninvasive Measure of Left Ventricular Filling Pressure in Heart Failure

Progressive left ventricular (LV) dysfunction induces expression of the cytokine transforming growth factor-β1. Endoglin (CD105) is a transforming growth factor-β1 co-receptor that is released into the circulation as soluble endoglin (sEng). The objective of the present study was to assess the serum levels of sEng in patients with heart failure and to identify the predictive value of sEng for detecting elevated left ventricular end-diastolic pressures (LVEDPs). We measured the sEng levels in 82 consecutive patients with suspected LV dysfunction referred for determination of left heart filling pressures using cardiac catheterization. Among these subjects, the sEng levels correlated with the LVEDP (R = 0.689; p <0.0001), irrespective of the LV ejection fraction. Using a receiving operating characteristic curve, the sEng levels predicted an LVEDP of ≥16 mm Hg with an area under the curve of 0.85, exceeding the measured area under the curves for both atrial and brain natriuretic peptide, currently used biomarkers for heart failure diagnosis (atrial natriuretic peptide 0.68 and brain natriuretic peptide 0.65; p <0.01 vs sEng). In 10 subjects receiving medical therapy guided by invasive hemodynamic monitoring for heart failure, decreased a pulmonary capillary wedge pressure was associated with a reduced sEng level (R = 0.75, p = 0.008). Finally, compared to 25 healthy controls, the sEng levels were elevated in subjects with suspected LV dysfunction (3,589 ± 588 vs 4,257 ± 966 pg/ml, respectively, p <0.005) and correlated directly with the New York Heart Association class (R = 0.501, p<0.001). In conclusion, circulating levels of sEng are elevated in patients with increased LVEDP and New York Heart Association class, irrespective of the LV ejection fraction. sEng levels also decreased in association with a reduced cardiac filling pressure after diuresis. These findings have identified circulating sEng as a sensitive measure of elevated left heart filling pressures.

Proarrhythmic risk of embryonic stem cell–derived cardiomyocyte transplantation in infarcted myocardium

Cellular replacement strategies using embryonic stem cells (ESCs) and their cardiac derivatives are emerging as novel experimental therapeutic paradigms for the treatment of post-myocardial infarction (MI) left ventricular (LV) dysfunction; however, their potential proarrhythmic risk remains unclear. The purpose of this study was to investigate the functional effect and proarrhythmic risk of ESC transplantation in a mouse model of MI. We compared the functional effects and proarrhythmic risk of direct intramyocardial transplantation of 3 × 10(5) undifferentiated mouse ESCs (MI+ESC group, n = 33) and mouse ESC-derived cardiomyocytes (MI+ESC-CM group, n = 40) versus culture medium (MI group, n = 33) at the infarct border zone in a mouse model of acute MI. LV performance was assessed with serial cardiac magnetic resonance imaging (MRI) at 1 and 3 week(s) post-MI, and invasive LV pressure measurement was assessed (dP/dt) at 4 weeks before sacrifice for histological examination. Furthermore, electrophysiological study was also performed in another set of animals in each group (n = 24) to assess for proarrhythmias after transplantation. In vitro cellular electrophysiological study demonstrated that ESC-CMs exhibit arrhythmogenesis including automaticity, lengthened action potential duration, and depolarized resting membrane potential. At 4 weeks, the MI+ESC-CM group (21/40, 53%) had a higher mortality rate compared with those in the MI group (10/33, 30%, P = .08) and in the MI+ESC group (7/33, 21%, P = .012). Electrophysiological study showed a significantly higher incidence of inducible ventricular tachyarrhythmias in the MI+ESC-CM group (13/24, 54%) compared with in the MI group (6/24, 21%, P = .039) and in the MI+ESC group (5/24, 21%, P = .017). Cardiac MRI showed similar improvement in LV ejection fraction in the MI+ESC and MI+ESC-CM groups compared with in the MI group at 1 week (27.5% ± 3.8%; 30.3% ± 5.2% vs. 12.4% ± 1.4%; P < .05) and 3 weeks (29.8% ± 3.9%; 27.0% ± 4.8% vs. 10.6% ± 2.8%; P < .05) post-MI, respectively. Furthermore, invasive hemodynamic assessment at 4 weeks showed significant similar improvement in LV +dP/dt in the MI+ESC (2,644 ± 391 mmHg/s, P < .05) and MI+ESC-CM groups (2,539 ± 389 mmHg/s; P < .05) compared with in the MI group (2,042 ± 406 mmHg/s). Our results demonstrate that transplantation of undifferentiated ESCs and ESC-CMs provides similar improvement in cardiac function post-MI. However, transplantation of ESC-CMs is associated with a significantly higher prevalence of inducible ventricular tachyarrhythmias and early mortality than transplantations with ESCs.

The relative contribution of prosthetic gradients, systemic arterial pressure, and pulse pressure to the left ventricular pressure in patients with aortic prosthetic valves

aortic valve replacement (AVR) in patients with aortic stenosis reduces the left ventricular (LV) pressure and the LV mass. However, residual LV hypertrophy at follow-up is a common finding with negative prognostic impact. In the present study, we investigate the contribution of the prosthesis (size, type, and gradients) and the load opposed by the arterial system to the mean LV pressure (MLVP). twenty-five patients with a bileaflet mechanical (n = 12, size 19-27) or stented biological (size 21-25) valve were included. After weaning from bypass, continuous Doppler recordings (transoesophageal transducer) and simultaneous LV and aortic pressure measurements were performed (high-fidelity catheters). The mean prosthesis gradients with catheter or Doppler were moderately correlated to MLVP (R(2) = 0.40 and 0.34, P = 0.002 and <0.0001). In a multiple regression model, the relationship between MLVP and prosthesis gradient, mean blood pressure, and pulse pressure was strong for both mechanical and biological valves. Using catheter prosthesis gradients, we could explain 97% of the variability in MLVP and when using Doppler gradients 91%. in the present study of patients with aortic prosthetic valves, we demonstrate the importance of the load opposed by the arterial system for the LV pressure. Our findings suggest that the MLVP can be estimated from easily obtainable Doppler data and blood pressure measurements. In analysing predictors of LV mass regression, morbidity, and mortality following AVR, the equations might be of interest.

Evaluation of cardiac contractility by left ventricular pressure measurement in telemetered beagle dogs

Evaluation of cardiac contractility by left ventricular pressure measurement in telemetered beagle dogs

Differential effects of sevoflurane and propofol anesthesia on left ventricular–arterial coupling in dogs

General anesthetics interfere with arterial and ventricular mechanical properties, often altering left ventricular-arterial (LVA) coupling. We hypothesized that sevoflurane and propofol alter LVA coupling by different effects on arterial and ventricular properties. Experiments were conducted in six anesthetized open-chest dogs for the measurement of left ventricular pressure and aortic pressure and flow. Measurements were performed during anesthesia with 0.5, 1.0 and 1.5 minimum alveolar concentration sevoflurane and 12, 24 and 36 mg/kg/h propofol. LVA coupling was assessed as the ratio of ventricular end-systolic elastance (E(es), measuring ventricular contractility) to effective arterial elastance (E(a), measuring ventricular afterload). The steady component of afterload, arterial tone, was assessed by systemic vascular resistance and arterial pressure-flow curves. The pulsatile component of afterload was assessed by aortic impedance and compliance. Sevoflurane decreased aortic pressure and cardiac output more than propofol. Sevoflurane reduced arterial tone, increased arterial stiffness and did not affect wave reflections. It increased E(a), decreased E(es) and reduced LVA coupling. Propofol reduced arterial tone, did not affect arterial stiffness and decreased wave reflections. It did not affect E(a), E(es) or LVA coupling. Sevoflurane increased ventricular afterload and decreased ventricular performance, thereby altering LVA coupling. Propofol did not affect ventricular afterload or ventricular performance, thereby preserving LVA coupling. Thus, propofol preserves LVA coupling in dogs better, and might be a better choice for patients with compromised left ventricular function.

Left Ventricular Pressure Measurement by Telemetry Is an Effective Means to Evaluate Transplanted Heart Function in Experimental Heterotopic Cardiac Xenotransplantation

Evaluation of the function of heterotopic cardiac transplants has traditionally been accomplished by either manual palpation or serial biopsies. Both methods have drawbacks. Palpation can be difficult to differentiate a pulse from the graft versus a transmitted pulse from the native aorta. Serial biopsies, though accurate, require multiple laparotomies, leading to increased morbidity and possibly mortality rates. In this study we used an advanced telemetry system, consisting of an intra-abdominal implant, that was capable of continuously monitoring simultaneously several parameters of the transplanted heart and the status of the recipient. In a large animal model of heterotopic cardiac xenotransplantation (pig donor to baboon recipient), we implanted the device in 12 animals: 8 with and 4 without immunosuppression. We monitored and continuously recorded the left ventricular pressure (both peak-systolic and end-diastolic [LVEDP]), heart rate, and the electrocardiogram pattern of the transplanted heart as well as the temperature of the recipient. The left ventricular pressure proved to be the most valuable parameter to assess graft heart function. In the 4 nonimmunosuppressed cases, grafts were rejected acutely. In these cases, the end-diastolic pressure increased sharply and the heart stopped contracting when the difference between the systolic and the diastolic pressure decreased to <10 mm Hg. The earliest reproducible sign of rejection was an increased LVEDP. Among long-term survivors, the increase in diastolic pressure was gradual, indicating progressive thickening of the myocardium and decreased compliance of the ventricle. Six of 8 immunosuppressed animals died of other complications before rejecting the transplanted heart. The telemetry was also helpful to indicate early onset of fever in the recipients, thus allowing us to intervene early and prevent potentially lethal septic complications. Continuous monitoring of several parameters via telemetry allowed detection of changes associated with rejection as well as other complications at an early stage, allowing prompt intervention, treatment, and possibly reversal of rejection.