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PubMed1990

Effect of static exercise and muscle ischemia on cardiac function as evaluated by the systolic time intervals.

To determine the role of muscle chemoreflex in the cardiac response to static exercise the effect of the forearm muscle ischemia on systolic time intervals (STI), heart rate (HR) and blood pressure (BP) recovery following static handgrip was studied in 7 healthy men. During handgrip maintained for 4 min at 30% maximal voluntary contraction HR and BP increased significantly while duration of the pre-ejection period (PEP) and isovolumic contraction time (ICT) were shortened with a significant lowering in the ratio of PEP to the left ventricle ejection time (LVET). Occlusion of the circulation to the forearm muscles for 2 min after cessation of exercise did not prevent a rapid decline of HR or increment in PEP, ICT and PEP-to-LVET ratio while BP remained elevated for as long as blood flow to muscles was restricted. The study failed to demonstrate an appreciable effect of muscle chemoreflex on HR or myocardial contractility, suggesting that input from muscle afferents activated by metabolic stimuli induces the pressor response mainly by the peripheral vasoconstriction.

Adult↗
PubMed1996

Donor-specific HLA antibodies after transplantation are associated with deterioration in cardiac function.

Although there is increasing evidence that mismatched donor HLA antigens are associated with a lowering of survival of human cardiac allografts, the effect of antibodies that bind those antigens is less clear. The existence of lymphocytotoxic antibodies prior to cardiac transplantation has been associated with a poor outcome in the majority of reports of relevant studies, as has their appearance post-transplantation. But how such antibodies, especially those with HLA specificity, cause poor outcomes has been poorly understood. The purpose of this study was to investigate the effect of anti-HLA antibodies appearing in the circulation after human orthotopic heart transplantation. Such antibodies were identified by a standard microlymphocytotoxicity technique using panels of frozen lymphocytes from normal donors who had been tissue typed. Of 74 patients transplanted over a 12-month period, 4 (5.4%) developed alloantibodies specific for mismatched donor HLA antigens. The first patient developed antibodies to HLA-A23 and B44 together with poor ventricular function and vascular rejection requiring retransplantation within 4 months. The other patients (3) developed antibodies specific for HLA-DQ antigens and experienced variable numbers of episodes of cellular rejection with no evidence of vascular rejection on endomyocardial biopsy. Two of these three patients died (8 and 11 months post-transplant) after three and six rejection episodes, respectively. The one surviving patient had seven rejection episodes and continues to have poor ventricular function 18 months post-transplant. We conclude that alloantibodies specific for mismatched donor HLA antigens may have a deleterious effect on the outcome of the human cardiac allograft and should be monitored closely post-transplant. Furthermore, such antibodies may mediate effects on the transplanted heart which are not detectable in specimens obtained by endomyocardial biopsy.

Adult↗
PubMed1998

Pattern of changes over time in myocardial blood flow and microvascular dilator capacity in patients with normally functioning cardiac allografts.

This study tests the hypothesis that myocardial blood flow and coronary microvascular dilator capacity vary as a function of time after orthotopic heart transplantation in humans. Positron emission tomography measurements of myocardial blood flow were obtained at rest and during adenosine in 24 patients between 1 and 86 months after heart transplantation. At the time of the study all patients were clinically well and had angiographically normal epicardial coronary artery vessels. Patients were divided into 3 groups based on time from transplant to positron emission tomography measurement of myocardial blood flow: group 1 to 12 months (n = 9); group 13 to 34 months (n = 8); and group > or = 37 months (n = 7). Basal myocardial blood flow in group 1 to 12 months (1.86+/-1.01 ml/min/g) exceeded (p <0.05) that of group 13 to 34 months (1.17+/-0.73) and group > or = 37 months (0.98+/-0.34). In group 13 to 34 months, basal myocardial blood flow and maximal dilator capacity (minimal coronary vascular resistance with adenosine 36+/-12 mm Hg/ml/min/g) were comparable to that of normal volunteers (1.01+/-0.20 and 37+/-, respectively). In group > or = 37 months, maximal flow response to adenosine was reduced (2.54+/-1.25 vs 3.16+/-0.52, respectively, p = 0.06). Maximal dilator capacity in group > or = 37 months (60+/-34) was impaired versus group 1 to 12 months (36+/-10) and group 13 to 34 months (36+/-12; both p <0.05) as well as normals (37+/-9, p <0.05). During the first year after cardiac transplantation basal myocardial blood flow is elevated out of proportion to external determinants of myocardial oxygen demand, but maximal dilator capacity of the coronary microcirculation is normal. Between 1 and 3 years both basal myocardial blood flow and microvascular function tend to normalize. After 3 years, although basal myocardial blood flow is normal, microvascular dilator capacity is impaired.

Adult↗
PubMed2001

Altered cardiac function.

An understanding of the normal functioning of the heart and how it fails is important since it allows rational treatment. Pre-existing cardiac disease and myocardial dysfunction is common in the surgical patient. Moreover, the stress response of surgery and the alterations in body physiology seen in the post-operative period may further aggrivate any cardiac compromise. The end result may be a patient who has cold peripheries due to vasoconstriction and hypoperfusion with dyspnoea due to congested lungs and a heart that cannot function adequately. The postoperative patient is at risk of these changes because of the stress response, analgesic therapy, inappropriate fluid management, hypoxia and previous cardiac compromise. The patient with sepsis is at further risk because of alterations in both systolic and diastolic function, which may be the result of inadequate fluid resuscitation and also release of a variety of inflammatory mediators. Until treatments, which are aimed at correcting the effects of these mediators, are proven to be beneficial then the septic patient will continue to be managed according to the physiological principles as outlined by Starling.

Cardiac Output, Low↗
PubMed1996

Electrophysiologic abnormalities of cardiac function in progressive systemic sclerosis.

The heart has been generally recognized as a target organ in progressive systemic sclerosis. Noninvasive studies have assessed the incidence and prognostic importance of cardiac arrhythmias in these patients. However, detailed exploration of the function of impulse formation and the conduction system of the heart in these patients has never been reported. Therefore, invasive electrophysiologic studies were performed in 30 patients with systemic sclerosis, all of whom had neither obvious cardiac involvement nor cardiac arrhythmias, and in 32 subjects with no evidence of heart disease, who served as a control group. Corrected sinus node recovery time in patients with systemic sclerosis was significantly longer (P < .001) than in the control group, as was the HV interval (P < .05). Of the 30 patients with systemic sclerosis, 10 had an HV interval of 60 ms or longer. In four patients with systemic sclerosis, the recorded AH interval exceeded 125 ms. The intra-atrial conduction time tended to increase to a significant degree (P < .05) in patients with systemic sclerosis. The interatrial conduction time was much longer (P < .001), and the maximal conduction delay to the atrioventricular junction and to the distal coronary sinus was much greater in the patients with systemic sclerosis than in the control group (P < .001 for both). Supraventricular tachyarrhythmias were induced in 15 patients with systemic sclerosis versus 3 control group subjects (P < .001). With respect to corrected sinus node recovery time, AH and HV intervals, atrial vulnerability, and ventricular tachycardia, 3 of the 30 patients with systemic sclerosis had abnormal findings in one of these parameters and 14 had abnormalities in more than one. These results suggest that a broad spectrum of electrophysiologic abnormalities is present in patients with systemic sclerosis, which can be revealed only by invasive studies. Furthermore, this study provides additional support for the hypothesis that diffuse myocardial involvement is characteristic of scleroderma patients, since a number of these patients showed more than one electrophysiologic defect.

Adolescent↗
PubMed1984

Results of radionuclide assessment of cardiac function following transplantation of the heart.

Radionuclide assessment of ejection fraction was determined early and late postoperatively following cardiac transplantation in 16 patients. In 11 patients, ejection fraction was determined within 48 hours of an endocardial biopsy. There was no relationship between the severity of histologically evident rejection and the ejection fraction (Pearson correlation coefficient [r] = -0.11; p = 0.47). In 2 patients, severe graft fibrosis developed with consequent diminution in ejection fraction. There was no relationship between severity and duration of rejection or the amount of immunosuppression required to treat acute rejection and the development of graft fibrosis. The mean resting ejection fraction in 7 patients in follow-up ranging from 6 to 21 months after transplantation was 0.59 +/- 0.06 (standard deviation), and the mean exercise ejection fraction in 6 of these patients was 0.72 +/- 0.08. Radionuclide-determined ejection fraction is not predictive of rejection early after operation. During short-term late follow-up, systolic left ventricular function at rest and exercise has been retained at normal levels.

Heart↗