BACKGROUND The exercise-induced rise in left ventricular filling pressures after cardiac transplantation is considered to be the result of a blunted heart rate response, of elevated venous return, and of unfavorable passive late-diastolic properties of the cardiac allograft. In contrast to passive late-diastolic left ventricular properties, the effect of left ventricular relaxation on the exercise-induced rise in left ventricular filling pressures of the cardiac allograft has not yet been studied. In the present study, the response of left ventricular relaxation to exercise was investigated in transplant recipients and compared with left ventricular relaxation observed in normal control subjects exercised to the same heart rate. Moreover, the response of left ventricular relaxation of the cardiac allograft to beta-adrenoreceptor stimulation, to reduced left ventricular afterload, and to increased myocardial activator calcium was investigated by infusion of dobutamine and of nitroprusside and by postextrasystolic potentiation. METHODS AND RESULTS Twenty-seven transplant recipients were studied 1 year (n = 17), 2 years (n = 7), 3 years (n = 2), and 4 years (n = 1) after transplantation. All patients were free of rejection and of significant graft atherosclerosis at the time of study. Tip-micromanometer left ventricular pressure recordings and cardiac hemodynamics were obtained at rest, during supine bicycle exercise stress testing (n = 27), during dobutamine infusion at a heart rate matching the heart rate at peak exercise (n = 8), during nitroprusside infusion (n = 9), and after postextrasystolic potentiation (n = 10). Tip-micromanometer left ventricular pressure recordings were also obtained in a normal control group (n = 9) at rest and during supine bicycle exercise stress testing to a heart rate, which matched the heart rate of the transplant recipient group at peak exercise. Left ventricular relaxation rate was measured by calculation of a time constant of left ventricular pressure decay (T) derived from an exponential curve fit to the digitized tip-micromanometer left ventricular pressure signal. In the transplant recipients, exercise abbreviated T from 43 +/- 6 to 40 +/- 8 msec (p less than 0.01) and caused a rise of left ventricular minimum diastolic pressure (LVMDP) from 5 +/- 2 to 9 +/- 6 mm Hg (p less than 0.001). In normal control subjects, exercise induced a 2.5 times larger abbreviation of T (from 42 +/- 7 to 34 +/- 6 msec; p less than 0.001) and a small drop in LVMDP from 5 +/- 2 to 4 +/- 3 mm Hg (p less than 0.05). In the transplant recipients, the change in T (delta T) from rest to exercise was variable ranging from an abbreviation, as observed in normal controls, to a prolongation and was significantly correlated with the change in RR interval (delta RR) and the change in left ventricular end-diastolic pressure (delta LVEDP) (delta T = 0.068 delta RR + 0.58 delta LVEDP-2.2; r = 0.76; p less than 0.001). In a first subset of transplant recipients (n = 8), dobutamine infusion resulted in a heart rate equal to the heart rate at peak exercise, a left ventricular end-diastolic pressure (8 +/- 7 mm Hg) lower than at peak exercise (22 +/- 6 mm Hg; p less than 0.05) and a T value (32 +/- 9 msec), which was shorter than both resting value (44 +/- 5 msec; p less than 0.005) and value observed at peak exercise (40 +/- 8 msec; p less than 0.01). In a second subset of transplant recipients (n = 9), nitroprusside infusion and postextrasystolic potentiation resulted in a significant prolongation of T from 41 +/- 7 to 56 +/- 10 msec (p less than 0.05) and a characteristic negative dP/dt upstroke pattern with downward convexity as previously observed in left ventricular hypertrophy. CONCLUSIONS Exercise after cardiac transplantation resulted in a smaller acceleration of left ventricular relaxation than in a normal control group exercised to the same heart rate...
Introduction: Although multiple defects of the atrial septum are not uncommon, there remain limited data regarding the use of multiple devices in these patients. A variety of approaches to transcatheter closure have been used, and in this paper we describe the experience from two operators in a single centre. Methods: From September 2002 to September 2012, 673 transcatheter atrial septal defects (ASD) and patent foramen ovale (PFO) closure procedures were performed and retrospectively examined in a registry analysis. Results: Of these, 22 patients had multiple discrete defects, and four different approaches to closure were used. In 4 patients (18.2%) one device was used percutaneously to close multiple defects. Eleven patients (50%) had two devices inserted during the same procedure while two patients (9%) had two devices inserted as staged procedures. One patient (4.5%) had three devices inserted over two procedures. Four patients (18.2%) were found not to be suitable for percutaneous closure during the procedure and were referred for surgical closure. Conclusion: Our experience with the implant procedures, and clinical follow up of patients, shows that patients with multiple defects can be effectively treated with transcatheter device techniques including single device closure, multiple devices in one procedure and multiple devices in staged procedures and also with surgical repair.
Glyceryl trinitrate (nitroglycerin) has been in use for relief of angina for over a hundred years, but allergic reactions to it or to other organic nitrates rarely feature in the medical literature. Most of the case reports describe reactions to transdermally applied nitroglycerin. We report a case of a localized allergic reaction to nitroglycerin transdermal patches that developed when these were worn for the first time after 7 days of uneventful treatment with intravenous isosorbide dinitrate. The reaction evolved into a severe and generalized maculopapular rash with facial swelling when intravenous isosorbide dinitrate was re-administered 10 days later. Subsequent patch testing with a transdermal nitroglycerin patch and a placebo nitroglycerin-free patch provoked a reaction to the nitroglycerin patch but not to the placebo, thus excluding allergy to other constituents of the nitroglycerin patch.
The purpose of the study was to evaluate whether infusion of a beta-adrenergic agonist, prior to and during exercise, could compensate for reduced sympathetic stimulation and correct deficient acceleration of left ventricular relaxation, so preventing a rise in left ventricular filling pressures during exercise after cardiac transplantation. Abnormal left ventricular relaxation kinetics can contribute to exercise-induced diastolic dysfunction of the cardiac allograft. This was demonstrated in transplant recipients whose acceleration of left ventricular relaxation during exercise was almost negligible recently and whose elevation of left ventricular end-diastolic pressure was high. Decreased adrenergic tone due to denervation could be involved in deficient left ventricular lusitropic response to exercise, because acceleration of left ventricular relaxation during exercise depends on adequate sympathetic stimulation. Serial supine bicycle exercise was performed at an identical workload in eight transplant recipients while in the control state and during continuous infusion of dobutamine, titrated before exercise to achieve a heart rate matching the heart rate at peak exercise in the control state. During control exercise, heart rate rose from 87 +/- 8 to 104 +/- 12 beats.min-1 (P < 0.05), left ventricular end-diastolic pressure from 14 +/- 5 to 20 +/- 4 mmHg (P < 0.05), left ventricular dP/dtmax from 1374 +/- 172 to 1854 +/- 278 mmHg.s-1 (P < 0.05), and cardiac output from 5.8 +/- 0.9 to 8.5 +/- 1.1 l.min-1 P < 0.05). There was a small but significant decrease of the time constant of left ventricular pressure decay (T) from 42 +/- 6 to 38 +/- 6 ms (P < 0.05). During dobutamine infusion, exercise resulted in a further increase in heart rate from 108 +/- 11 to 122 +/- 17 mmHg (P < 0.05), in cardiac output from 7.4 +/- 0.9 to 10.3 +/- 2.5 l.min-1 (P < 0.05), and in left ventricular dP/dtmax from 2181 +/- 220 to 2620 +/- 214 mmHg.s-1 (P < 0.05). These values were higher than the measurements obtained at the end of the control exercise run (P < 0.05). T failed to change (29 +/- 4 vs 27 +/- 5 mmHg, P > 0.05) and left ventricular end-diastolic pressure increased from 5 +/- 3 to 11 +/- 5 mmHg (P < 0.05) but remained lower than at the end of the control exercise run (11 +/- 5 vs 20 +/- 4 mmHg, P < 0.05). Compensation for reduced sympathetic stimulation by administration of dobutamine improves exercise haemodynamics in cardiac transplant recipients, but cannot prevent the exercise-induced rise in left ventricular end-diastolic pressure and correct deficient acceleration of left ventricular relaxation. Abnormal exercise haemodynamics after heart transplantation are therefore only partly related to deficient sympathetic stimulation.
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