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Biomedical subjects

J Koller-Strametz

Publications and source records attributed to J Koller-Strametz.

18 recordsLinked to original sources

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

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

[Modified surgical technique for reduction of bone marrow spilling in cement-free hip endoprosthesis].

Since 1970 the fat embolism syndrome (FES) has been recognised as a severe complication of cemented total hip arthroplasty (THA). Initially and still today the toxicity of bone cement has been though to be responsible for the cardiorespiratory problems. Meanwhile several reports have confirmed the causal relationship between intramedullary pressure (IMP), bone-marrow release into the circulation and subsequent cardiorespiratory deterioration during cemented THA. In recent publications it has been reported that bone-marrow release due to increased IMP also occurs during cementless THA. The clinical implication of these observations is controversial. For this reason in the first part of this paper two autopsy-proven FES deaths and five further clinically manifest FES cases are presented. In the second part of the study, IMP courses during four different surgical techniques (2 conventional, 2 modified) are compared. The aim of the modified surgical technique developed in our department was to minimize IMP peaks and bone-marrow release during cementless THA. Both modified techniques showed significantly lower IMPs during opening of the medullary canal, preparation with rasps, and implantation of the prosthesis than the conventional techniques. The observed FES cases for the first time strongly confirm the clinical relevance of the FES, also during cementless THA. On the basis of the data presented we recommend the modified surgical technique to reduce bone-marrow release during cementless THA.

Aged

[Modified surgical technique for the reduction of bone marrow spilling in knee endoprosthesis].

In the literature 20 cases of fat embolism syndrome (FES) after total knee replacement (TKR) are reported; 16 cases had cemented hinged TKR and 4 resurfacing TKR. Initially, it was believed that the bone cement was responsible for the FES. Since then, however, Fahmy et al. have published extraordinary data, demonstrating the causal relationship between increased intramedullary pressure (IMP) during the insertion of the intramedullary rod (IR) and cardiorespiratory deterioration. The industry responded by developing a fluted IR, disregarding the overdrilling in the distal femur required by Fahmy. In the first part of this paper clinically manifest FES cases after resurfacing TKR are reported. In the second part of the study the conventional surgical technique is compared with a modified technique, which focuses on a reduction of bone-marrow release into the circulation. In the conventional and the modified group, IRs with and without flutes were compared. It was shown that only the opening of the intramedullary canal and insertion of the IR generated relevant IMP peaks during implantation of resurfacing TKR. When compared with the conventional surgical technique, the modified technique revealed significantly lower IMPs, and in neither group was a difference demonstrated between the IR with or without flutes. In 4 patients (2 conventional, 2 modified) transesophageal echocardiography (TEE) was performed for detection of bone-marrow release into the circulation. In the two patients operated on conventionally, TEE showed a markedly higher bone-marrow release than in the patients with modified operations. In conclusion, we recommend the presented modified surgical technique in order to reduce bone-marrow release into the circulation.

Aged

[Therapeutic approach to the management of fat embolism syndrome].

So far, no clinical or experimental study has demonstrated that any drug has a beneficial effect (heparin, cortisone, dextran, etc.) on the course of fat embolism syndrome (FES). Thus, prevention, early diagnosis, and adequate symptomatic treatment are of paramount importance. Besides surgical measures, such as reduction of intraosseous pressure and bone-marrow release during hip or knee replacement, proper treatment of shock in traumatized patients, recognition of risk factors and maintainance of intraoperative cardiorespiratory stability are cornerstones in the prevention of fat embolism syndrome. It is well documented that bone-marrow release into the circulation and pulmonary embolism occurs during any hip or knee arthroplasty. As a result of improvements in anesthesia management, the clinical appearance of FES has moved into the postoperative period. This calls for mandatory cardiorespiratory monitoring up to 24 h postoperatively. When facing a clinically manifest fat embolism syndrome, monitoring and symptomatic treatment must be adapted to the patient's needs in order to ensure adequate oxygenation and acceptable circulatory conditions to protect organ function.

Catheterization, Swan-Ganz

[Pathophysiology of fat embolisms in orthopedics and traumatology].

It is well known that fat embolisms can occur after long bone fractures, and this has been feared for more than 100 years. Since 1970 fat embolisms have also been recognized in endoprosthetic surgery. The clinical manifestation was described as the fat embolism syndrome (FES) by Gurd in 1974. Based on reports in the literature and our own data, a concise pathophysiological model of the FES is presented in this paper. The increase in intramedullary pressure (IMP) in the long bones is the most decisive pathogenic factor for the development of an FES. Any long bone fracture, stabilization of fractures, or implantation of knee or hip endoprostheses can generate IMP peaks leading to bone marrow release into the circulation. Bone marrow itself is a tremendous stimulus for activation of the clotting system. As a result, hypercoagulation and venous stasis in the draining veins generate mixed macroemboli from the initial bone-marrow microemboli. Bone-marrow embolization of the lung in phase I leads to mechanical obstruction of pulmonary arteries. In phase II, release of local mediators, triggered by a systemic inflammatory response (SIR) of the lungs, causes damage to the pulmonary membranes. Disturbed gas exchange and respiratory insufficiency with possible cardiac and cerebral decompensation are the result. In most cases an FES may not be detected clinically, and any mild cardiorespiratory changes are treated easily with oxygen insufflation and usually disappear within 48 h. Of paramount importance for clinical manifestation of an FES are the quantity and duration of bone-marrow release and co-factors (cardiorespiratory compliance and perioperative stability of the patient). Patients with preexisting cardiorespiratory disease in combination with massive intraoperative bone-marrow release may even face a deadly FES event. Increased IMP causes local obstruction of cortical vessels with bone marrow. In combination with the damaged endosteal blood supply, avascular necrosis of the cortical bone occurs. During endoprosthetic procedures, mechanical-and mediator-triggered damage of the intima of big veins, in combination with venous stasis and hypercoagulation may be responsible for the high incidence of proximal thrombosis of femoral veins. As a delayed result of the disseminated intravascular coagulopathy, petechial bleeding in the trunk and subconjunctiva can be seen. A better understanding and recognition of the FES's pathophysiology may help to use prophylactic, diagnostic and therapeutical measures more effectively.

Blood Coagulation

Primary hyperparathyroidism and the heart: cardiac abnormalities correlated to clinical and biochemical data.

Comparing patients with primary hyperparathyroidism (PHP) to a normocalcemic control population, those with PHP have a higher incidence of cardiovascular disease and cardiac abnormalities. This study aimed at correlating cardiac findings (valvular and myocardial calcification, myocardial hypertrophy) with clinical data (age, sex, clinical manifestation, nephrolithiasis, nephrocalcinosis, hypertension, skeletal abnormalities, hypercalcemic syndrome) and biochemical data (serum calcium, serum phosphate, serum iPTH level, serum creatinine). A group of 132 consecutive patients with surgically verified PHP (94 women, 38 men; ages 15-86, mean age 57 +/- 16 years) were included in this study. Blood chemistry, clinical presentation, radiography, and echocardiography were carried out in all patients for univariate and multivariate analyses of all parameters. There was no statistical correlation between clinical symptoms, biochemical data, and cardiac calcific alterations. Typical skeletal manifestations (osteolysis/subperiostal resorption) and valvular calcifications were significantly correlated to left ventricular hypertrophy (p = 0.005). Cardiac abnormalities such as calcific myocardial deposits or mitral and aortic valvular calcifications do not correlate with laboratory findings and clinical presentation at the time of diagnosis. There was no biochemical or clinical variable that could predict the frequency or severity of valvular sclerosis or calcific deposits in the myocardium. However, PHP-related skeletal abnormalities and valvular calcification were predicting factors for left ventricular hypertrophy, a reversible cardiac manifestation of PHP. Myocardial hypertrophy is more often found with classic symptomatic PHP with osseous abnormalities.

Adolescent

Thromboembolism associated with junctional escape rhythm and atrial standstill after orthotopic heart transplantation.

We report on thromboembolism in a heart transplant recipient with mechanical atrial standstill and spontaneous echocardiographic contrast during intermittent periods of sinus arrest and junctional escape rhythm. The temporal relationship between the conversion of atrial flutter to junctional bradycardia and two episodes of thromboembolism strongly suggest a role of the lack of atrial contraction during junctional rhythm for the development of spontaneous echocardiographic contrast and thromboembolism.

Arrhythmias, Cardiac