SUMMARY Cardiac arrhythmias, myocardial necrosis and ECG abnormalities in stroke may result from abnormally high levels of sympathetic activity. To examine this possibility, plasma norepinephrine, epinephrine and dopamine were measured in 74 patients with cerebral infarction, 18 with transient ischemie attacks and 33 non-stroke controls.Mean norepinephrine, epinephrine and dopamine values (pg/ml) in cerebral infarction (433.2, 81.6, 57.6) were higher (p < 0.01) than in controls (281.1, 60.1, 40.5, respectively). Transient ischemie attacks produced values intermediate to these two groups (319.3, 80.9, 54.9). The elevated catecholamine concentrations in cerebral infarction could not be explained by differences in age, blood pressure, heart rate, stress, type or severity of stroke. The high plasma norepinephrine in the stroke group is consistent with an increase in peripheral sympathetic activity which could produce the cardiac abnormalities of cerebral infarction.

SUMMARY Serum cardiac enzyme levels (CK, LDH, SCOT) were estimated and the ECG recorded for 4 days following admission of 288 patients (Group I) to a stroke intensive care unit. Sixty-four of these patients, subsequently found not to have strokes, served as controls. Mean serum levels of all 3 cardiac enzymes were elevated in 8% of the 224 patients with stroke. The mean serum enzyme levels in patients with transient ischemic attacks (TIA) did not differ from controls.In a second group of 230 patients with stroke (Group II) serum CK levels were measured and the isoenzymes were fractionated to determine the tissue source of the enzymes. One hundred and one patients had raised total CK values and 25 of these (11%) had raised CK-MB (heart) iso-enzyme, the remainder having CK-MM (skeletal muscle) fraction. No serum CK-BB (brain) iso-enzyme was detected in any patient. Patients with positive serum levels of CK-MB had more evidence of acute myocardial ischemia on ECG (p < 0.05), and more cardiac arrhythmias (p < 0.001) than those with normal CK levels. Scattered areas of myocytolysis were found in the myocardium at autopsy in one patient.The acute rise in serum cardiac enzymes which we have recorded in the initial stages of stroke suggest that acute myocardial involvement is a commoner complication than is generally recognized. Also, since the CK-MB rises were modest and progressive, it is more likely that this acute myocardial dysfunction is a consequence, rather than a cause, of the acute cerebrovascular lesion.

Blood pressure (BP) readings in the doctor's office are mean awake ambulatory BP. Mean (± s.e.m.) routine office BP (mm Hg) recorded by the patient's physician frequently higher than home or ambulatory values. This study examines the role of the physician in the aetiology (155 ± 4/80 ± 2) was similar to the mean value obtained using the automated BP recording device of the 'white coat' effect, by comparing standard readings taken by the family physician of 27 treated hyper-(157 ± 3/83 ± 2). The mean awake ambulatory BP was 145 ± 3/78 ± 2 with the systolic value lower (P Ͻ Ͻ Ͻ 0.05) tensive patients with readings taken by an automated BP recording device, with the patient alone in the examthan either the physician or automated reading. Selfmeasurement of BP by the patient in the office setting ining room during the same office visit. The physician and automated readings were each compared to the does not reduce the magnitude of the white coat effect.Keywords: blood pressure; self measurement; white coat effect individuals already receiving antihypertensive ther- Introduction apy. Patients frequently exhibit an increase in bloodOne factor in the measurement of office BP has pressure (BP) when visiting their physician's office, not yet been examined in the clinical setting -does a phenomenon which has been called the 'white the presence of a physician in the examining room coat' effect. A variety of factors have been shown to affect the level of a patient's BP? The present study increase office BP compared to ambulatory readings addresses this question by comparing routine BP during usual daily activities. BP increases upon the readings taken by the patient's family physician arrival of the patient in the doctor's office and tends using a mercury sphygmomanometer with readings to diminish during the subsequent 10 min. 1 Convertaken by an automated BP recording device with the sation with the patient also tends to accentuate the patient resting alone in the examination room. Both white coat effect. 2 Office BP and the consequent the automated and physician readings were also white coat effect may be reduced by having a nurse compared to the ambulatory BP to see if the use of record the office BP. 1,3 Digit preference, the use of an automated device could reduce any white coat aneuroid sphygmomanometers and unfamiliar sureffect which might be present. roundings for new patients may also contribute to higher office readings and the misdiagnosis of Patients and methodshypertension. 4 The white coat effect has usually been considered Patient population as part of the diagnosis of patients with possiblePatients were recruited from the computerised rechypertension. In previous studies 5,6 we have also ords of a family practice unit in a university teachnoted a persistent difference between office and ing hospital (Sunnybrook Health Science Center). A ambulatory readings in patients receiving long-term random sample of 45 treated hypertensive patients antihypertensive therapy from their own family were identified. Initi...

SUMMARY The blood pressure and plasma norepinephrine response to oral tyrosine, the precursor of norepinephrine, supplementation (2.5 g t.i.d.) of regular meals was examined in 13 untreated patients with mild essential hypertension. Using a randomized double-blind crossover design, each 2-week treatment was followed by a 2-week supplement-free interval. Supine and standing blood pressure and plasma norepinephrine levels were measured at the beginning and end of each 2-week treatment. Plasma tyrosine levels increased (p< 0.001) from 71.2 ± 8.0 nM/ml at baseline to 152.8 ± 17.4 nM/ml 2 hours after the tyrosine supplement. Blood pressure under control conditions was 144 ± 3 mm Hg systolic, 91 ± 2 mm Hg diastolic (109 ± 2 mm Hg mean) after 30 minutes in the supine position and 148 ± 4 mm Hg systolic, 102 ± 3 mm Hg diastolic (117 ± 3 mm Hg mean) after 5 minutes of standing. Plasma norepinephrine levels were 191 ± 18 pg/ml in the supine subjects and 390 ± 33 pg/ml in the standing subjects. No differences in systolic, diastolic, or mean blood pressure, heart rate, or plasma norepinephrine levels were seen between the beginning and end of each period or between groups. Individual changes in blood pressure showed no correlation with individual changes in norepinephrine levels. These results indicate that the addition of a tyrosine supplement to the usual diet of mild hypertensive subjects has no beneficial effect on blood pressure. (Hypertension 7: 593-596, 1985) KEY WORDS • plasma norepinephrine • diet • amino acid • catecholamines T

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At least six epizootics of simian hemorrhagic fever have occurred at four different primate centers. Although these diseases could easily be transmitted to other monkeys of the Macaca species, difficulty has been encountered in isolating the causative virus in cell culture. The results of this study have shown that the isolation of simian hemorrhagic fever virus strains in cell culture is dependent upon the use of a susceptible MA-104 cell strain and that the ability of such strains to support the replication of these viral agents may vary. By using this information we have been able to isolate a viral agent in cell culture from materials derived from the Sussex/69 epizootic.

In patients with hypertension persisting on combined diuretic and beta-blocker therapy, the effects of an additional 9-week therapy with a calcium antagonist (nifedipine) versus a classical arterial vasodilator (hydralazine) were compared for changes in blood pressure (BP), plasma catecholamines (n = 15), and left ventricular (LV) systolic and diastolic function (n = 6). Both drugs lowered BP, but nifedipine was significantly more effective in lowering systolic BP. Hydralazine increased both supine and standing plasma norepinephrine, nifedipine increased them only in the standing position and to a lesser extent. Patients on beta1-selective (n = 5) versus nonselective (n = 10) blockade showed similar responses. Left ventricular systolic function was not affected by hydralazine, whereas nifedipine increased the rate of ejection. In contrast, LV diastolic function was not affected by nifedipine, whereas hydralazine improved the peak filling rate. We conclude that arterial vasodilation by a calcium antagonist causes less sympathetic activation than caused by a classical arterial vasodilator. However, during short-term therapy in patients already on a diuretic and a beta blocker, nifedipine appears not to improve decreased LV diastolic function.

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