A patient with polycythemia.
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Biomedical subjects
Publications and source records attributed to K F Hossack.
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A system of computer terminals was set up in a group of office practices, industrial medical departments and hospitals and connected to a central computer. This service provides a means of analyzing treadmill exercise results, which are displayed graphically on the computer printout. The system also provides estimates of probabilities of primary or secondary coronary heart disease events developing based on the exercise responses.
Whereas hypertension is a risk factor for primary coronary heart disease events, the relative contributions of other risk factors and abnormal responses to symptom-limited maximal exercise are not well-established. After 5.2 +/- 1.5 years of follow-up of 633 men with clinically-diagnosed hypertension based upon criteria of examining physicians (whether or not the men were currently treated for hypertension), 54 primary events were revealed. The annual coronary heart disease (CHD) event rate of 16.9/1000 men at risk was significantly higher than the annual rate of 3.6/1000 found for healthy men (p < 0.0001). Variables associated with increased risk were smoking cigarettes, risk factor count or tally, chest pain during exercise, percentage of functional aerobic impairment, and percentage heart rate impairment, the latter two variables suggesting early evidence of left ventricular dysfunction on strenuous exertion. Ischemic ST depression was not an important predictor. The three exercise variables were included in an exercise predictor count, and multivariate analysis revealed that this count and the risk factor count were the most important predictors of primary CHD events. Combining the risk factor count and the exercise predictor count, three groups with increasing risk of primary CHD events were identified. In those persons with both a risk factor count and exercise predictor count of zero, the annual rate was 7.3 events/1000 man-years; when either count was one or more, the rate was 15.5 events/1000 man-years; when both counts were one or more, the rate was 49.5 events/1000 man-years.
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Two hundred and eighteen patients with congenital valvar aortic stenosis aged between 1 and 25 years at presentation were followed for one to 26 years (average 8.7 years). Assessment of severity of aortic stenosis was essentially based on clinical findings including symptoms, the character of the pulse, and the behaviour of the second heart sound, management being further influenced by the degree of left ventricular hypertrophy shown in the electrocardiogram. There was reasonable correlation between clinical and haemodynamic assessment and all patients with a gradient between left ventricle and aorta (LV-Ao) greater than 50 mmHg (6.7 kPa) were judged to have moderate or severe aortic stenosis on physical signs. Fifty-five per cent of those judged mild on presentation still had a mild lesion 18 years later; 42 per cent of those judged moderate on presentation still had a moderate lesion 15 years later. Forty-four patients had an operation and of the 30 patients who underwent aortic valvotomy, only 40 per cent still had a satisfactory result 13 years later. There were three preoperative and seven postoperative deaths but in only two patients was death directly related to severe aortic stenosis and both of these patients had been lost to follow-up. It is concluded that indications for operation are aortic stenosis which is moderate or severe on physical findings, together with restrictive symptoms or ST and T wave changes on the electrocardiogram. Using these criteria, the risk of sudden death is minimal and irreversible myocardial damage unlikely. We do not recommend either routine cardiac catheterisation or routine operation at any arbitrary LV-Ao gradient.
Review of a longitudinal study of the effects of 40 mg of propranolol orally in 14 patients with coronary heart disease demonstrated a minor but not statistically significant change in the relationship of percentage of maximal oxygen uptake to percentage of maximal heart rate. In a cross-sectional comparison of several hundred patients who showed no other significant difference in initial findings in relation to propranolol, significant differences were present with respect to resting heart rate and responses to symptom-limited exercise, nevertheless the relationship of percentage of maximal oxygen uptake to the percentage of maximal heart rate was similar. Accordingly, we recommend maximal exercise testing in all patients prior to undertaking an exercise program so that their maximal heart rate can be determined accurately and rational training heart rates advised. The exercise test should be performed with the patients taking medications they anticipate continuing during the period of physical training, and if a change in medications is subsequently made then the exercise test should be repeated.
9 patients with clinically manifest ischemic heart disease underwent hemodynamic and electrocardiographic monitoring at rest, during several levels of submaximal and near maximal exercise on a treadmill and in recovery. The observations were repeated following infusion of mannitol. Despite augmentation of cardiac output at near maximal exercise, the electrocardiographic evidence of ischemia worsened.
A mailed questionnaire was sent to 2,892 men aged 35-65 years who had undergone symptom-limited treadmill exercise testing. The study was designed to assess the possible role of exercise testing as a means of motivating patients to modify appropriate risk factors and health habits. There was a 69% response to the questionnaire and 63% of patients replying indicated they modified one or more risk factors and health habits and this change they attributed to the exercise test. It was found that persons with an abnormal functional aerobic impairment, demonstrated by the exercise test, were more likely to be motivatged to change. This pilot study raises the possibility that exercise testing may play an important role in modification of coronary risk factors and health habits and the design of a better controlled study is suggested.
In 12 patients with symptomatic coronary heart disease and three normal persons, comprehensive analyses of the electrocardiographic changes associated with symptom-limited upright exercise are made by computer analysis of the electrocardiogram recorded using a Frank XYZ lead system. This analysis provided a display of the 12 lead ECG, vectorcardiogram, polarcardiogram, and spatial cardiogram and measurements of spatial magnitudes of heart vectors. The effect of 40 mg of oral propranolol was assessed by repeating the exercise protocol 60--90 min later. There is evidence that propranolol reduces the electrocardiographic features of myocardial ischemia. This reduction in myocardial ischemia correlates with reductions in pressure rate product and heart rate. The presence of infarct criteria with exercise is variable and not apparently influenced by propranolol.
Treadmill exercise testing was performed on 23 patients with isolated congenital aortic stenosis. It was found that eight patients, with a negative exercise test and a normal rise in systolic blood pressure on exercise, had gradients less than 45 mmHg. Fifteen patients with gradients greater than 50 mmHg had positive exercise tests and their systolic blood pressure did not rise normally. It is suggested that the left heart studies to measure aortic valve gradients can safely be postponed if an exercise test is negative. Serial exercise testing of such patients will give an indication when left heart catheterization should be considered.
The functional result of aortic valve replacement has been assessed in patients treated for isolated aortic incompetence. Using maximal oxygen uptake as an index of myocardial function, a significant difference (p less than .05) exists between the patients who had Q fever endocarditis on the one hand and those who had bacterial endocarditis or rheumatic fever on the other hand. We believe that permanent myocardial damage occurs as a result of bacterial endocarditis and rheumatic fever but because of the biological properties of Coxiella burnetii the myocardium is spared in Q fever endocarditis.
Five hundred and eighty-eight patients with mitral valve disease were studied. The incidence of systemic emboli was found to be higher in patients with pure mitral stenosis (16.6%) and mixed mitral stenosis and incompetence (19.4%) than in patients with mitral incompetence (3.1%). The patients with mitral stenosis who had episodes of systemic emboli tended to be older than 40 years, with moderate or severe valve lesions, atrial fibrillation and moderate or gross enlargement of the left atrial appendage or left atrium. The following factors were found to be unrelated to systemic embolism---associated aortic valve disease, sex, smoking habit, history of rheumatism, parity, haemoglobin, blood urea, pulmonary hypertension, duration of antifailure treatment, presence of heart failure, and cardiothoracic ratio.
A case of subvalvular aortic stenosis in one of a set of dissimilar twins is reported. The case is discussed in terms of the aetiological factors involved and supports the view that supravalvular aortic stenosis is not environmental and may be genetic in origin.
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Six of 85 patients (7%) with alcoholic liver disease undergoing transhepatic portal pressure measurement had either stagnant (3 patients) or reversed (3 patients) portal blood flow documented by gentle hand injection of 1 to 2 ml of angiographic contrast. Portal blood flow was uniformly hepatopetal in 24 patients with nonalcoholic liver disease. Recurrent spontaneous hepatic encephalopathy and sodium retention occurred in 4 of 6 patients with stagnant or reversed portal flow; gastrointestinal bleeding was not seen. Standard laboratory tests of liver function were widely variable. Net portal pressure was lower in this group than in patients with alcoholic liver disease and forward portal flow (9.2 +/- 2.6 vs. 15.6 +/- 4.1 mm Hg, p less than 0.001). Wedged hepatic vein pressure was 1 to 7 mm Hg higher than portal vein pressure in patients with reversed portal flow. The arterioportal extraction of bile acid was calculated from the difference in concentration between artery and portal vein, and total functional hepatic blood flow was calculated from the hepatic extraction and systemic clearance of indocyanine green. Extraction was 0%, and hepatic blood flow was 0.469 liter per min in a patient with hepatofugal portal flow and recurrent encephalopathy. Extraction was 20%, and hepatic blood flow was 4.014 liters per min in a patient who had never had encephalopathy. These data indicate that arterioportal communications may be sinusoidal or presinusoidal in patients who lose forward portal flow and that the amount of flow in the arterioportal circuit, together with its efficiency, largely determine the clinical outcome.
Sudden unexplained death syndrome (SUDS) accounts for about 10% of deaths in patients with epilepsy. It is associated with subtherapeutic postmortem serum antiepileptic drug (AED) levels but no anatomic cause of death on autopsy. The mechanisms of death are not known. We investigated 44 cases of SUDS for details of seizure history, treatment, medical and psychological history, events at the time of death, and postmortem findings. Cases of status epilepticus, drowning or other identifiable causes of death were excluded. Two groups emerged: five children with uncontrolled seizures receiving multiple AEDs and good compliance with medications, and 39 adults with less frequent seizures, often receiving monotherapy, but noncompliant with medications. Four children (80%) but only one adult (3%) had fully therapeutic postmortem AED levels. Sixty-three percent of adults recently had experienced an unusually stressful life event. Investigation of the circumstances at the time of death suggested two possible modes of death: (a) a seizure with an immediately fatal arrhythmia, or, (b) a seizure, recovery, then delayed secondary respiratory arrest or arrhythmia. Even though the mechanisms of death are unknown, the risk of SUDS may be reduced by encouraging patients to be compliant with medications, especially in times of unusual life stress.
One hundred patients, eighty-nine men and eleven women, with chronic stable angina who were previously selected for aortocoronary bypass grafting gave informed consent for non-invasive and invasive testing of hemodynamic responses to symptom-limited maximal exercise before surgery. Psychosocial coping strategies were evaluated preoperatively by structured interviews and assessment of patients perceptions of symptoms (Cornell Medical Index) and life changes (Holmes and Rahe Schedule of Recent Experiences). Preoperatively forty-one patients were "compartmentalized," forty-two "generalized" and seventeen "vacillated" according to Josten's classification of coping strategies. The Berle Index of social assets was lower and the prevalence of psychiatric symptoms (Cornell categories M to R) was greater in the vacillators preoperatively. Despite less ischemic ST depression in vacillators, no other significant physiological differences were noted between these categories preoperatively. Postoperatively more of the vacillators refused follow-up evaluation, and of vacillators who returned, only one-half were adequately revascularized at operation. Of sixty-five reevaluated after surgery, eight improved, twelve worsened and forty-five did not change classification of coping strategies, yet physiological variables of cardiac function when invasively measured in sixty patients were significantly improved in all three groups. Amounts of improvement, both absolutely and relative to sex- and age-adjusted normal values, were least in vacillators with virtually normal cardiac capacity, and/or inadequate revascularization. Compartmentalized patients were more frequently working, yet only sixty-four in all psychosocial classifications worked before surgery. After this event only forty-five resumed working; none of the non-workers or retired returned to work. Both physiologic improvement and working status were independent of postoperative psychosocial status.