Pulmonary and Systemic Hemodynamics in Patients with Hyperthyroidism.

BACKGROUND: There is an association between hyperthyroidism and pulmonary hypertension. However, the prevalence of pulmonary hypertension in hyperthyroidism and the underlying mechanisms are incompletely defined. METHODS: Consecutive patients with severe hyperthyroidism, mostly due to Graves disease, were included in this single-center study. Echocardiographic assessment of pulmonary hemodynamics was performed at the time of hyperthyroidism diagnosis (baseline) and after normalization of thyroid hormones (follow-up; median 11 months). In a subset of patients, right heart catheterization and noninvasive assessment of central hemodynamics was performed. RESULTS: Among all 99 patients, 31% had pulmonary hypertension at baseline. The estimated systolic pulmonary artery pressure correlated significantly with the estimated left ventricular filling pressure (E/e'). The invasively measured systolic pulmonary artery pressure correlated well with the estimated systolic pulmonary artery pressure. Cardiac output, E/e', left and right ventricular dimensions were significantly reduced from baseline to follow-up, whereas the estimated pulmonary vascular resistance did not differ. Diastolic blood pressure was significantly higher at follow-up, with no change in systolic blood pressure. The central systolic blood pressure, however, exhibited a trend for a reduction at follow-up, while the pulse wave velocity was significantly lower at follow-up. CONCLUSIONS: Approximately one-third of patients with hyperthyroidism have evidence of pulmonary hypertension. Our data suggest that an increased cardiac output and left ventricular filling pressure are the main mechanisms underlying the elevated systolic pulmonary artery pressure in hyperthyroidism, whereas there is no evidence of significant pulmonary vascular disease.

Short-term high altitude exposure at 3454 m is well tolerated in patients with stable heart failure.

AIMS: High altitude exposure for the purpose of tourism is very popular in mountainous regions and is considered to be safe for patients with stable CAD and preserved LV function. The purpose of this study was to evaluate the haemodynamic response to exercise and electrical stability by Holter monitoring in patients with chronic heart failure (HF) and an EF <40%. METHODS AND RESULTS: We studied 29 HF patients with a peak VO2 >50% of the predicted (25 men, age 60.0 ± 8.9 years, EF 28.8 ± 5.4%) at 540 and 3454 m after an ascent using public transport. Assessments of exercise capacity (cardiopulmonary exercise test), haemodynamic response (inert gas rebreathing system), and susceptibility to arrhythmias (Holter ECG recording) were performed. None of the patients (19 with ischaemic heart disease, 11 with an implantable cardioverter defibrillator) had to return prematurely to the lowland site. Two patients presented symptoms of mild mountain sickness, and one patient developed a self-limited ventricular tachycardia during maximal exercise at high altitude. Mean peak VO2 at the lowland site was 18.5 ± 3.6 mL/min/kg and decreased by 22.2% (P < 0.001) at high altitude. Mean resting heart rate increased from 74.3 ± 12.3 to 83.3 ± 13.4 b.p.m., P < 0.001. No statistically significant difference in premature ventricular contractions (92 ± 150/h at 540 m vs. 111 ± 196/h at 3454 m, P = 0.284) was noted. CONCLUSION: Patients with stable chronic HF and a peak VO2 >50% of the predicted tolerate a short exposure to an altitude of 3454 m well, even during exercise. However, it cannot be excluded that the susceptibility to ventricular tachyarrhythmias during exercise is increased in some subjects.

Randomised trial of a clinical dosing algorithm to start anticoagulation with phenprocoumon.

QUESTION UNDER STUDY: Prospective validation of two algorithms for the initiation of phenprocoumon treatment. METHODS: Inpatients with new-onset anticoagulation were randomised to one of two computer assisted dosing algorithms, or to a control arm. The primary outcome measure was the time to achieve therapeutic anticoagulation without overshooting (INR >4.0 within 10 days). Secondary outcomes included overshooting INR values, death, or bleeding within 30 days. In addition, predictors of the dosing algorithms for the loading dose and the maintenance dose including genetic parameters were reassessed. RESULTS: 105 patients were randomised to arm A, 103 to arm B and 93 to the control arm. Arms A and B needed a median of 7 days to reach a therapeutic INR, arm C 6 days (p = 0.5). Overshooting INR was observed in 3.8%, 1.9% and 4.3% respectively (p = 0.6). Bleeding was found in 0%, 1.9%, and 5.4% (p = 0.06) and 30-day mortality was 0%, 1%, and 2.2% respectively (p = 0.2). VKORC1:c.-1639 G>A was associated with lower loading doses whereas VKORC1:c.-1453 G>A needed higher doses. VKORC1:c.-1639 G>A was also associated with lower maintenance doses. CONCLUSION: Both algorithms allow safe initial dosing of phenprocoumon but they are not superior to anticoagulation by trained physicians. Dosing aids for coumarins with readily available clinical parameters may nevertheless be helpful for use in polymorbid hospitalised patients. Clinical data and the INR-response to treatment provides powerful information and delaying initiation of anticoagulation while awaiting genetic tests is not expected to increase drug safety.

Superior temporal gyrus differences in childhood-onset schizophrenia.

The posterior superior temporal gyrus (STG) is the approximate site of Wernicke's area, a language region, which in previous studies has been reported to be abnormal in adults with schizophrenia. The present study assesses volumetric differences in the superior temporal gyrus of subjects with childhood-onset schizophrenia (COS). MRI scans of 18 subjects diagnosed with childhood-onset schizophrenia and 16 age- and sex-matched normals were analyzed to assess possible volume differences. The COS subjects displayed significant enlargement of the right posterior superior temporal gyrus, showing white matter increases bilaterally in this region. Our findings are consistent with studies that have found increased volumes in temporal lobe regions in COS and may provide a possible neural correlate for the language impairment observed in COS patients.

Nontraumatic pancreatitis in spinal cord injury.

STUDY DESIGN: A retrospective analysis of 10 patients with pancreatitis after traumatic spinal cord injury. OBJECTIVES: To determine the conditions leading to nontraumatic pancreatitis in spinal cord injury. SUMMARY OF BACKGROUND DATA: Little is known in the literature about pancreatitis after spinal cord injury. A few authors suggest a multifactorial pathogenesis. METHODS: Over a 4-year period the case reports of 338 patients with traumatically caused SCI were reviewed concerning p-amylase and/or lipase elevations. Acute pancreatitis was defined as an elevation of p-amylase and/or lipase of more than three times the upper normal limit. RESULTS: Ten of 338 patients had p-amylase and/or lipase elevations three times higher than the upper normal limit. All 10 were male with a mean age of 40.4 years. The average onset time of acute pancreatitis was 16 +/- 5.5 days after trauma. The usual etiologic factors of acute pancreatitis such as obstructive, toxic, or traumatic events were excluded. CONCLUSION: The clinical recognition of acute pancreatitis in paraplegic and quadriplegic patients is hampered by diminished or lost visceral sensitivity and therefore is based on laboratory investigations. The current authors therefore hypothesize that acute pancreatitis in the setting of high-level spinal cord injury may result from a combination of locally mediated sphincter of Oddi dysfunction and vagal dominant innervation of the pancreatic gland in autonomic failure.