Elevation of prostatic markers following cardiogenic shock.
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Acid Phosphatase↗
Biomedical subjects
J Koller-Strametz
Publications and source records attributed to J Koller-Strametz.
Elevation of prostate-specific markers after cardiopulmonary resuscitation.
BACKGROUND-Prostate-specific antigen (PSA), acid phosphatase (AP), and prostatic acid phosphatase (PAP) are serum markers for adenocarcinoma of the prostate gland. Previous studies indicated that prostatic ischemia may also produce elevations of PSA. Cardiopulmonary resuscitation (CPR) is frequently associated with profound tissue hypoperfusion. The present study investigated whether PSA, AP, and PAP are influenced by prolonged CPR. METHODS AND RESULTS-PSA, AP, and PAP were assessed immediately, 12 hours, 24 hours, 2 days, 3 days, 5 days, and 7 days after prolonged CPR (>5 minutes) in 14 male and 5 female patients. No changes were noted in women. In men, serum levels increased significantly after CPR and gradually decreased to near baseline values after 7 days. PSA, AP, and PAP values above the normal range were observed in 63%, 71%, and 64% of all patients, respectively. Compared with survivors, nonsurvivors exhibited higher peak serum levels of PSA (98.6+/-14.3 versus 1.1+/-2.2 mcg/L; P<0.03), AP (57.0+/-71 versus 8.6+/-8.8 U/L; P<0.05), and PAP (47.0+/-62 versus 5.7+/-8.0 U/L; P=NS). Patients with poor neurological outcome exhibited higher peak serum levels of PSA (86.4+/-135.5 versus 12.0+/-23.8 mcg/L; P<0.05), AP (50.9+/-68.1 versus 8.7+/-9.6 U/L; P=NS), and PAP (41.6+/-59.5 versus 5.8+/-8.8 U/L; P=NS) than patients with good neurological outcome. CONCLUSIONS-Prolonged CPR is frequently associated with increases of PSA, AP, and PAP serum levels. Therefore, PSA cannot be used for diagnosis of adenocarcinoma of the prostate during the first weeks after CPR. Further evaluation of these parameters as additional prognostic markers after CPR is warranted.
Acid Phosphatase↗
Milrinone therapy in catecholamine-dependent critically ill patients with heart failure.
BACKGROUND: Treatment with the PDE-III inhibitor milrinone improves hemodynamics in patients with heart failure. We examined whether therapy with milrinone is safe and effective in critically ill patients with catecholamine-dependent heart failure and whether treatment with milrinone facilitates weaning from prolonged catecholamine therapy. METHODS: Twenty adult patients with reduced left ventricular function and prolonged (7+/-4 days) catecholamine therapy in whom attempts at catecholamine weaning had failed were examined. Patients were prospectively randomised either to group A (addition of a fixed dose of 0.5 microg x kg(-1) x min(-1) milrinone to catecholamine therapy) or to group B (continued catecholamine therapy without milrinone). Dobutamine and norepinephrine treatment and fluid intake were titrated according to predefined hemodynamic goals. Hemodynamic parameters, fluid requirements and catecholamine dose were monitored. RESULTS: After 24 h of study treatment goup A showed a significant increase in cardiac index (2.2+/-0.4 1 min(-1) x m(-2) to 2.7+/-0.51 min(-1) x m(-2); P<0.005), a decrease in systemic vascular resistance (1,427+/-609 dyn x s x cm(-5) to 951+/-184 dyn x s x cm(-5); P<0.005), required lower doses of dobutamine (5.9+/-4.2 microg x kg(-1) x min(-1) to 2.2+/-3.3 microg x kg(-1) x min(-1); P<0.02), but showed a tendency for higher vasoconstrictor (0.14+/-0.16 microg x kg(-1) x min(-1) to 0.29+/-0.43 microg x kg(-1) x min(-1); P=n.s.) and fluid requirements (+1,404+/-2,257 ml/24 h to +2,508+/-1,873 ml/ 24 h; P=n.s.). No significant changes occurred in group B. Weaning from catecholamine therapy was more often achieved in group A and more milrinone treated patients were discharged alive from the ICU (80% vs. 30%; P<0.05). CONCLUSIONS: Milrinone improves central hemodynamics and may facilitate weaning from prolonged catecholamine support in critically ill patients with heart failure. Its administration in this subset of critically ill patients is safe, but eventually is associated with additional vasoconstrictor and fluid requirements.
Aged↗
Soluble selectins and the systemic inflammatory response syndrome after successful cardiopulmonary resuscitation.
OBJECTIVE: Elevated cytokine levels have been reported after ischemia/reperfusion injury and might cause a systemic inflammatory response syndrome (SIRS) after successful cardiopulmonary resuscitation (CPR). It is unknown whether patients with SIRS after CPR exhibit higher levels of soluble adhesion molecules than patients without SIRS and whether SIRS or elevation of adhesion molecules is associated with outcome after CPR. We analyzed the relationships among various CPR-related variables, plasma levels of E- and P-selectin, the occurrence of SIRS after CPR, and the development of sepsis and outcome. DESIGN: Prospective, controlled study. SETTING: Intensive care unit at a university hospital. PATIENTS: A total of 25 patients on the second day after successful CPR and 7 non-critically ill control patients. INTERVENTIONS: Blood sampling for determination of plasma levels of soluble (s) E- and P-selectin. MEASUREMENTS AND MAIN RESULTS: SIRS was a frequent finding after CPR (66% of all patients) unrelated to time until return of spontaneous circulation (SIRS, 17+/-13 mins; no SIRS, 19+/-16 mins; p = .761), epinephrine dose (SIRS, 4+/-5 mg; no SIRS, 5+/-6 mg; p = .906), or serum lactate level after CPR (SIRS, 8.6+/-2.6 mmol/L; no SIRS, 8.7+/-4.0 mmol/L; p = .174). sP-selectin levels were higher in patients with SIRS (291.7+/-227.4 ng/mL) compared with patients without SIRS (113.4+/-88.4 ng/mL; p = .018) or with non-critically ill patients (116.9+/-33.4 ng/mL; p = .031). Compared with non-critically ill control patients (42.8+/-19.4 ng/mL), sE-selectin levels were higher in patients with (96.2+/-47.3 ng/mL; p = .023) and without SIRS (99.5+/-65.7 ng/mL; p = .030). sP-selectin was higher in patients developing sepsis within 1 wk after CPR (n = 9) than in patients without sepsis (350.2+/-233.4 ng/mL vs. 158.5+/-157.8 ng/mL; p = .022) and sE-selectin levels were higher in nonsurvivors (n = 5) than in survivors (144.2+/-62.4 ng/mL vs. 85.7+/-45.3 ng/mL; p = .025) whereas SIRS was unrelated to the development of sepsis (p = .4) and unrelated to survival (p = .4). CONCLUSIONS: SIRS is an unspecific finding after CPR with only minor impact on outcome. Determination of sP- and sE-selectin early after CPR might help to identify patients at a high risk for sepsis or for an adverse outcome, respectively.
Adult↗
Renal hemodynamic effects of L-arginine and sodium nitroprusside in heart transplant recipients.
BACKGROUND: Long-term treatment with cyclosporine A (CsA) induces vasoconstriction in the kidney and causes renal impairment. An altered L-arginine (L-Arg)/nitric oxide (NO) pathway may play a key role in CsA nephrotoxicity. METHODS: We studied the effect of L-Arg (dosage, 17 mg/kg/min over 30 min), the precursor of NO synthesis, and sodium nitroprusside (SNP; dosage, 1.0 microgram/kg/min over 30 min) on renal hemodynamics in a double-blind, placebo-controlled, randomized, three-way cross-over study comprising 12 stable cardiac transplant recipients on long-term CsA treatment, 10 patients with chronic nephropathy not receiving CsA, and 13 healthy controls. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured by paraaminohippurate (PAH) and the inulin clearance method, respectively. RESULTS: In healthy subjects, L-Arg induced an increase in RPF (P = 0.009) and GFR (P = 0.001). By contrast, L-Arg did not induce renal hemodynamic effects in heart transplant patients or patients with chronic nephropathy. SNP reduced RPF (P = 0.050) and GFR (P = 0.005) in patients with chronic nephropathy but did not affect renal hemodynamics in heart transplant recipients or in healthy subjects. CONCLUSIONS: These data indicate that L-Arg cannot be used to reverse CsA-induced renal vasoconstriction in heart transplant recipients under long-term CsA treatment, although these patients have a normal renal response to SNP.
Aged↗
Fibrinolytic response to venous occlusion compared to physical stress test in young patients with coronary artery disease.
INTRODUCTION: Venous occlusion (VO) and exercise stress (ES) are stimulators of the fibrinolytic system. Aim of this study was to answer which of both stimulation tests is more useful in patients with symptom-limited coronary artery disease (CAD) to evaluate possible defects in the fibrinolytic system. METHODS AND RESULTS: We investigated 20 patients (M/F = 15/5; mean age = 36.7 years) with angiographically proven CAD for their plasma levels of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-type-1 (PAI-1) at basal conditions as well as after VO and at maximal ES (standardised bicycle stress test) and compared the data to those obtained from 12 sex- and age-matched healthy controls (M/F = 9/3; mean age = 40.4 years). At basal conditions mean t-PA activity and t-PA antigen plasma levels were within the normal range and comparable between the two study groups. After both VO and maximal ES, mean t-PA activity and t-PA antigen levels increased significantly more in the control group as compared to the CAD group. Mean PAI-1 activity plasma levels were significantly higher in the CAD group at basal conditions before VO (patients 7.0 +/- 3.1; controls 3.9 +/- 3.9; IU/ml; p = 0.025) as well as before ES (patients 8.1 +/- 3.5; controls 4.3 +/- 3.8; IU/ml; p = 0.009). PAI-1 activity plasma levels showed a significant decrease for patients and controls only after VO, while PAI-1 activity was not significantly decreased in both study groups at maximal ES. DISCUSSION: The significantly higher increase in mean plasma levels of t-PA activity and t-PA antigen after VO compared to ES in both groups might be explained by the fact that CAD induced symptoms in the patients during ES thus permitting only 80% of their age, sex, and body mass index related optimal work load. CONCLUSION: VO and ES are applicable triggers of the endogenous fibrinolytic system in healthy subjects and patients who are not limited in their physical exercise. Standardised VO appears to be superior to ES as stimulation test of the endogenous fibrinolytic system in patients with symptomatic CAD.
Adult↗
Role of nitric oxide in exercise-induced vasodilation in man.
Nitric oxide (NO) is a potent endothelium-derived vasodilator, which is known to play an important role in the regulation of resting vascular tone in animals and humans. However, the degree to which NO is involved in exercise-induced vasodilation in the skeletal muscle remains unclear. We studied the effect of N-monomethyl-L-arginine (L-NMMA) in a randomized, double-blind, placebo controlled cross over study in 16 young, healthy volunteers ( 8 male, 8 female) at rest and during bicycle exercise stress test. L-NMMA was given as a bolus of 3 mg/kg over 5 minutes followed by a continuous i.v. infusion of 50 microg/kg/min over 75 minutes. Subjects underwent a symptom-limited graded bicycle stress test with a 25 Watt increase in workload every 5 minutes. Skin and muscle blood flow were measured by laser Doppler flowmetry. L-NMMA slightly increased mean arterial blood pressure and decreased NO exhalation, but had no effect on pulse rate, oxygen consumption (VO2), skin or muscle blood flow at rest. Moreover, L-NMMA exerted no effect on exercise-induced changes in hemodynamics. Our results suggest that submaximal inhibition of NO-synthase with L-NMMA at doses that induce moderate hemodynamic changes does not affect exercise induced vasodilation.
Adult↗
Benign prognosis of early sinus node dysfunction after orthotopic cardiac transplantation.
Previous reports raised concern about the prognosis of patients with sinus node (SN) dysfunction after cardiac transplantation and led to a low threshold for permanent pacemaker (PM) placement at most institutions. The present study addresses the survival in patients with normal and impaired post operative SN function and the effect of permanent pacing with respect to overall and cardiac mortality. There were 120 patients with normal (corrected SN recovery time < 520 ms, group I) and 47 patients with imparied SN function (corrected SN recovery time > 520 ms and/or sinus arrest +/- escape rhythms). Pacing support was deemed unnecessary in 23 of 47 patients with SN dysfunction (group II; asymptomatic SN bradycardia and corrected SN recovery time 3,812 +/- 5,800 ms) while a total of 24 patients had PM placement a mean of 29 +/- 44 days after transplantation (symptomatic bradycardia or absence of sinus rhythm at discharge, group III). Patients were followed for a mean of 46.7 months. Thirty-five deaths occurred during the study period. Sixteen deaths were cardiac but none were causally related to the SN dysfunction (graft failure due to rejection or atheropathy n = 14; myocardial infarction n = 2). Four of these cardiac deaths were sudden and all occurred in the presence of widespread structural abnormalities (rejection/vasculopathy/myocardial infarction). SN dysfunction was not related to overall (P = 0.25) or cardiac mortality (P = 0.33). Regarding either endpoint, patients who had permanent PM placement did no better than their unpaced counterparts in group II (P = 0.53 and P = 0.33, overall and cardiac mortality, respectively). Likewise, survival did not differ between groups I and III for either endpoint (P = 0.77, P = 0.65, respectively). These data suggest that patients with mild SN abnormality, who are in sinus rhythm at the time of discharge, can be followed by observation without specific therapy.
Adult↗
Circulating tumor necrosis factor-alpha levels in chronic heart failure: relation to its soluble receptor II, interleukin-6, and neurohumoral variables.
The cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are increased in the circulation of patients with chronic heart failure. However, their correlation with left ventricular dysfunction has not yet been thoroughly evaluated, and their interrelation with other neurohumoral systems, such as the adrenergic system and endothelin, is unclear. Therefore TNF-alpha, its soluble receptor II, IL-6, big endothelin, and noradrenaline levels were simultaneously measured in venous blood from 65 patients with heart failure in New York Heart Association (NYHA) class II to IV during therapy with digitalis, furosemide, and enalapril. TNF-alpha plasma levels were 3.2+/-0.2 SEM pg/ml in 38 patients in NYHA function class II, 4.0+/-0.3 SEM pg/ml in 16 patients in NYHA function class III, and 5.3+/-0.9 SEM pg/ml in 11 patients in NYHA function class IV (p < 0.001 vs NYHA function class II). IL-6 plasma levels were 3.1+/-0.6 SEM pg/ml in 38 patients in NYHA function class II, 5.2+/-0.8 SEM pg/ml in 16 patients in NYHA function class III, and 13.3+/-3.9 SEM pg/ml in 11 patients in NYHA function class IV (p < 0.0001 vs NYHA function class II andp < 0.0001 vs NYHA class III). Thus both cytokines increased with increasing severity of heart failure, but only IL-6 plasma levels were different in patients in the more severe function classes. TNF-alpha correlated closely with TNF soluble receptor II (r = 0.8, p < 0.0001) and modestly with serum creatinine (r = 0.6, p < 0.0001), whereas IL-6 plasma levels were not statistically related to kidney function. Significant modest correlations were also found among TNF-alpha and IL-6 (r = 0.3, p < 0.01), big endothelin (r = 0.3, p < 0.01), and noradrenaline levels (r = 0.4, <0.001). This study supports the hypothesis that in heart failure both cytokines, TNF-alpha, and IL-6, as well as neurohumoral factors, play a role in the clinical progression of the disease. Thereby levels of TNF-alpha but not IL-6 seem to be related to concomitant kidney dysfunction.
Adrenergic Agonists↗
Effects of atenolol as add-on therapy to fosinopril in heart failure.
Several trials have demonstrated functional benefit with beta-blockers in patients with chronic heart failure. The aim of this observational study was to investigate if additional beneficial effects can be obtained from beta-blockade in a heart failure population that is already receiving high-dose ACE-inhibitor therapy. Atenolol is a long-acting cardioselective beta-blocking agent and is devoid of additional vasodilatory properties. Twenty-five male patients with class II or III heart failure and background therapy of digitalis, furosemide and 20 mg fosinopril per day were treated with 40 mg fosinopril per day and additional 75 mg atenolol per day (beta-blocker group) or with 40 mg fosinopril per day alone (control group). At the end of one year, changes in left ventricular function, exercise parameters and plasma neurohumoral variables reflecting vasoconstriction (noradrenaline, big endothelin) were measured and compared in the two treatment groups. Nineteen patients completed the study. Drop-outs were due to death (4 patients) and non-compliance (2 patients) with no significant difference between the groups. There was a beta-blocker related improvement in left ventricular ejection fraction (p < 0.05 between groups) and an increase in peak oxygen consumption in the control group only (p < 0.05 between groups). Thus, in a heart failure population receiving high-dose ACE inhibitor background therapy beta-blockade with atenolol produced additional benefit by reversing left ventricular dysfunction.
Adrenergic beta-Antagonists↗
[Aortic coarctation--long-term follow-up in adults].
Surgical repair of coarctation of the aorta has been performed since 1945. Although surgical techniques have improved, problems such as restenosis and aneurysm at the operation site or hypertensive cardiovascular disease, still remain. To evaluate the long-term results after surgical repair of coarctation, 41 patients, 25 male and 16 female patients (mean age: 28 +/- 11 years, range 14-57 years), were studied 16 +/- 8 years after surgery (range 3-44 years). Mean age at surgery was 12 +/- 9 years (range 0.5-35 years). In 24 patients resection and end-to-end anastomosis had been performed, patch graft aortoplasty in nine patients, tube interposition graft in seven patients and one patient had undergone the subclavian flap technique. All patients were assessed by exact physical examination, the resting arm-to-leg systolic pressure gradient was measured by Doppler sonography, a bicycle exercise test and an echocardiogram were performed. Twenty-one patients reported postoperative symptoms such as dizziness (n = 12), headache (n = 3), cold legs (n = 10) and/or dyspnea (n = 8). In two patients the resting arm-to-leg pressure gradient was greater than 30 mm Hg, in two patients it was greater than 20 mm Hg. Gradient calculated by Doppler echocardiography ranged from 0 to 80 mm Hg (21 +/- 17 mm Hg) and showed poor correlation with the arm-to-leg pressure difference. The mean functional capacity was 89 +/- 18% (range 42-110%). In 18 patients exercise-induced hypertension was found, while in only eight patients arterial hypertension had already been known. To evaluate the morphology of the aorta MRI was performed in 28 patients. No aneurysm was found. In five patients a minimal lumen diameter as small as 9-11 mm was measured. Patients were divided into two groups according to their age at operation, group I: < 9 years (n = 19) and group II: > 9 years (n = 22). Resting blood pressure was significantly higher in group II (135 +/- 27 mm Hg vs 114 +/- 20 mm Hg, p < 0.009), anti-hypertensive medication (43% vs 11%, p < 0.04) and symptoms were more frequent in these patients (15/22 vs 6/19, p < 0.04). However at time of follow-up examination the age of patients of group II was significantly higher (33 +/- 12 vs 22 +/- 5 years, p < 0.0005). Between these two groups there was no difference in follow-up time and results of echocardiography or stress test. In conclusion, despite good long-term results after surgical repair of coarctation of the aorta, patients should be followed on a regular basis primarily in order to recognize systemic hypertension as early as possible and to improve the long-term outcome in these patients by antihypertensive treatment.
Adolescent↗
Effects of physical training on heart rate variability in diabetic patients with various degrees of cardiovascular autonomic neuropathy.
OBJECTIVE: To investigate the effects of regularly performed endurance training on heart rate variability in diabetic patients with different degrees of cardiovascular autonomic neuropathy (CAN). METHODS: Bicycle ergometer training (12 weeks, 2 x 30 min/week, with 65% of maximal performance) was performed by 22 insulin-requiring diabetic patients (age 49.5 +/- 8.7 years; diabetes duration 18.6 +/- 10.6 years; BMI 25.1 +/- 3.4 kg/m2): i.e., by 8 subjects with no CAN, 8 with early CAN and by 6 patients with definite/severe CAN. A standard battery of cardiovascular reflex tests was used for grading of CAN, a short-term spectral analysis of heart rate variability for follow-up monitoring of training-induced effects. RESULTS: While the training-free interval induced no changes in spectral indices, the 12-week training period increased the cumulative spectral power of the total frequency band (P = 0.04) but to a different extent (P = 0.039) in different degrees of neuropathy. In patients with no CAN the spectral power in the high-frequency (HF) band (0.15-0.50 Hz) increased from 6.2 +/- 0.3 to 6.6 +/- 0.4 In [ms2]; P = 0.016, and in the low-frequency (LF) band (0.06-0.13 Hz) from 7.1 +/- 0.1 to 7.6 +/- 0.3 in [ms2]; P = 0.08 which resulted in an increase of total spectral power (0.06-0.50 Hz) from 7.5 +/- 0.1 to 8.0 +/- 0.3 in [ms2] (P = 0.05). Patients with the early form of CAN showed an increase of spectral power in HF (5.1 +/- 0.2 to 5.8 +/- 0.1 in [ms2], P = 0.05) and LF bands (5.6 +/- 0.1 to 6.3 +/- 0.1 in [ms2], P = 0.008), resulting in an increase of total power from 6.1 +/- 0.1 to 6.6 +/- 0.1 in [ms2] (P = 0.04), whereas those with definite/severe CAN showed no changes after the training period. Training improved fitness in the whole patient cohort. The increased autonomic tone as assessed by spectral indices disappeared after a training withdrawal period of 6 weeks. CONCLUSIONS: In diabetic patients with no or early CAN, regularly performed endurance training increased heart rate variability due to improved sympathetic and parasympathetic supply, whereas in subjects with definite/severe CAN no effect on heart rate variability could be demonstrated after this kind of training.
Autonomic Nervous System Diseases↗
Time course of regression of left ventricular hypertrophy after successful parathyroidectomy.
BACKGROUND: We have shown that primary hyperparathyroidism may induce myocardial hypertrophy that is reversible after successful parathyroidectomy. The present study was designed to assess the time course of regression of left ventricular hypertrophy without further effects of drug treatment or disease states. METHODS: We performed echocardiographic studies in 16 patients with primary hyperparathyroidism and normal resting blood pressure, normal systolic left ventricular function, no evidence of valvular disease, and without any current medication before parathyroidectomy, as well as during intermediate and long-term follow-up after successful parathyroidectomy. RESULTS: Eleven patients (69%) had end-diastolic wall thickness of the interventicular septum and/or posterior wall greater than 11 mm on baseline echocardiogram. After surgical removal of the inciting disease and an average of 12.5 and 45.7 months of follow-up with normocalcemia and normal parathyroid hormone levels a prolonged regression of left ventricular hypertrophy was observed (interventricular septum, -0.68 mm at 12.5 months and -1.69 mm at 45.7 months; p = 0.02; posterior wall, -0.46 mm at 12.5 months and -2.24 mm at 45.7 months; p = 0.02). CONCLUSIONS: We conclude that the removal of the cause of myocardial hypertrophy by successful parathyroidectomy leads to a prolonged reversal of hypertrophy. The progressive reduction of left ventricular wall thickness is not completed within 12 months.
Aged↗
PR interval adaptation in the denervated transplanted heart.
In the present study, the dynamic PR response upon standardized treadmill exercise was investigated in 21 transplant recipients (recipient age 48 +/- 17 years, donor age 31 +/- 12 years, > 1 year after transplantation). HR and PR interval were measured at rest and at the end of each 25-W increase in workload till peak exercise. In 17 cases norepinephrine (NE) was assessed at rest, and at the end of each workload the HR increased from 99.3 +/- 14 to 143.4 +/- 25 beats/min at individual peak exercise, and NE increased from 1,307 +/- 1,163 to 3,688 +/- 2,036 pg/mL, while the PR interval shortened from 149.2 +/- 13 to 119.3 +/- 20 ms. On average, PR decreased by 3.4 ms for a 10-beat increase in HR, and the HR-PR interval relationship was described by a linear regression (y = 176.8-0.3469x, P = 0.0001). One patient who was unable to increase his NE levels upon exercise showed virtually no decrease in the PR interval and no HR increase. Both recipient age and donor age were moderately and significantly related to the minimum PR interval achieved at peak exercise (r = 0.6, P = 0.008 and r = 0.51. P = 0.049, respectively). These data show the following: (1) adaptation of the PH interval upon exercise does occur in the denervated transplanted heart; (2) the HR-PR relation is similar to that reported in the innervated heart; (3) the overall decline in PR interval is blunted, since denervated patients start at shorter resting PR intervals and achieve relatively longer PR intervals at peak exercise when compared to their innervated counterparts; (4) these exercise induced changes of the PR interval may be explained by circulating NE; and (5) NE levels achieved at peak exercise and the sensitivity of the AV node to NE seem to be age related.
Adaptation, Physiological↗
Cardiac abnormalities in patients with primary hyperparathyroidism: implications for follow-up.
Patients with primary hyperparathyroidism (PHPT) show a high incidence of left ventricular hypertrophy, cardiac calcific deposits in the myocardium, and/or aortic and mitral valve calcification and thus may carry an increased risk of death from circulatory diseases. This prospective study was designed to assess an effect of parathyroidectomy on cardiac abnormalities of patients with PHPT. Echocardiography was used to evaluate the mechanical performance of the heart muscle, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications within 12 and 41 months after parathyroidectomy. In a blinded fashion, aortic and mitral value calcifications were determined in 46% and 39% of patients with PHPT. Calcific deposits in the myocardium were found in 74% of patients. Follow-up studies after parathyroidectomy disclosed no evidence of progression of these calcifications. Before operation left ventricular hypertrophy was detected in 82%. After parathyroidectomy and 41 months of normocalcemia and normal PTH concentrations, a regression of hypertrophy of the interventricular septum and the posterior wall by -6% and -19% (P < 0.05) was observed. Subgroup analysis disclosed the most impressive long-term reduction of left ventricular hypertrophy in patients without a history of hypertension (-11% and -21%; P < 0.05 and P < 0.005); no changes were determined in 9 patients who developed secondary hyperparathyroidism after operation. The present data show a high incidence of left ventricular hypertrophy and aortic and/or mitral valve calcifications in patients with PHPT. Follow-up at 1 year and at 41 months after successful parathyroidectomy disclose regression of hypertrophy. Our results give evidence that parathyroid hormone per se plays an important role in the maintainance of myocardial hypertrophy. Post-surgical restoration of normocalcemia and normalization of parathyroid hormone valvular sclerosis persists without evidence of progression. We further conclude that patients with PHPT and parathyroidectomy are at low risk for the development of severe aortic and mitral valve stenosis within this period of time.
Aged↗
Decrease in pacemaker incidence after orthotopic heart transplantation.
A decrease in sinus node dysfunction and pacemaker requirement after orthotopic heart transplantation was observed over a 6.5-year period, probably indicating the effect of a learning curve. Indirect evidence suggests a traumatic genesis of sinus node dysfunction after cardiac transplantation.
Arrhythmia, Sinus↗
Prognostic impact of big endothelin-1 plasma concentrations compared with invasive hemodynamic evaluation in severe heart failure.
OBJECTIVES: This study sought to test the hypothesis that big endothelin-1 plasma levels in advanced heart failure are related to survival. BACKGROUND: In heart failure, production of the potent vasoconstrictor endothelin-1 is increased. Because elevation of immunoreactive endothelin-1 in severe heart failure is primarily related to the precursor "big" endothelin-1, increased big endothelin-1 levels may be associated with a poor prognosis. METHODS: Plasma big endothelin-1 concentrations, in addition to 16 clinical, hemodynamic and neurohumoral variables, were obtained from 113 patients (mean age -=/[SEM] 53 +/- 1 years) with left ventricular ejection fraction <20% and were related to 1-year mortality by a stepwise Cox regression multivariate analysis. RESULTS: Plasma big endothelin-1 concentrations were significantly higher in patients with moderate and severe heart failure than in those with mild heart failure (4.5 +/- 0.4 and 6.0 +/- 0.1 vs. 2.7 +/- 0.1 fmol/ml, p = 0.0001, respectively) and lower in 58 one-year survivors than in 29 nonsurvivors (2.6 +/- 0.1 vs. 5.9 +/- .04 fmol/ml, p = 0.0001) and 26 heart transplant recipients. By univariate analysis, big endothelin-1 plasma concentrations (p < 0.0001), functional class, daily furosemide dose, left ventricular ejection fraction, most hemodynamic variables and plasma atrial natriuretic peptide, sodium renin activity and aldosterone levels were all related to mortality, but only functional class provided additional prognostic information when big endothelin-1 plasma levels were entered into the multivariate model. CONCLUSIONS: In advanced heart failure, plasma big endothelin-1 is strongly related to survival and appears to predict 1-year mortality better than hemodynamic variables and levels of atrial natriuretic peptide, an established neurohumoral prognostic marker in chronic heart failure.
Adult↗
[Monitoring of bone marrow spilling and cardiopulmonary changes in fat embolism syndrome].
After long bone fractures, as well as hip or knee total arthroplasty, the increase in intramedullary pressure induces bone marrow release into the circulation in more than 90% of patients. Three to four percent of the patients reveal fat embolism syndrome with pulmonary and cerebral involvement and a petechial rash. In about 20% of these patients a fulminant and fatal course is possible. Although fat embolism syndrome was described more than a century ago, there is still no sufficient therapeutic strategy. Because of these facts we try to prevent fat embolism syndrome and monitor patients at risk perioperatively. We have evaluated different diagnostic methods and monitoring facilities and recommend pulse oximetry, capnography, ECG, blood pressure controls and, if indicated, blood gas analyses for perioperative monitoring. Patients at risk and patients who are suffering from fat embolism syndrome require more intensive monitoring, such as transesophageal echocardiography and a pulmonary artery catheter to obtain more detailed information about the hemodynamic and oximetric variables. Furthermore, these patients must be admitted to an intensive care unit.
Blood Gas Analysis↗