Palliative care in terminal cardiac failure. Small numbers of patients with terminal cardiac failure may make considerable demands on services.
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Biomedical subjects
Publications and source records attributed to J M Beattie.
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There has been some debate on usefulness of the exercise test in risk stratification after myocardial infarction in the thrombolytic era. This was assessed in 295 patients of whom 184 were treated with thrombolysis. Each had an exercise test using a modified Naughton protocol within 14 days of acute myocardial infarction. The tests were graded as high risk positive (112), low risk positive (83), or negative (100). These gradings predicted use of multiple drug therapy (p = 0.05), severity of coronary artery disease (p < 0.01), and coronary artery bypass grafting (p < 0.01). There was no influence on heart failure, recurrent myocardial infarction or death. This was independent of the use of thrombolytic therapy. The whole group had a good prognosis with a mortality of 2.4% after 56 weeks' follow-up. The exercise test is still a useful screening test after myocardial infarction. In this study, there was a high negative predictive accuracy of 91% for any event. Its use is not altered by thrombolysis. The finding of a lack of influence of the exercise test on major events may be a reflection of the current good prognosis after myocardial infarction and the prompt use of revascularisation.
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The exercise test characteristics, coronary anatomy, and prognosis of patients discharged after non Q wave myocardial infarction were compared with those in whom Q wave infarction occurred. Of the 339 patients studied, all of whom were less than or equal to 70 years, 87 (26%) had had a non Q wave infarction. There were no significant differences in the exercise test characteristics between the two groups, and in those 149 patients in whom angiography was performed triple vessel disease was present in 36/114 (32%) of the Q wave group and 9/35 (26%) of the non Q wave group. The infarct related artery was more often patent in the non Q wave group (27/35 (77%] than in the Q wave group (53/114 (46%]. The one year mortality and the reinfarction and angina rates were similar in the two groups and the exercise test remained a good discriminator for predicting patients at risk of future cardiac events in both groups. In view of the similar outcome and severity of coronary disease in those aged less than or equal to 70 with non Q wave infarcts, the distinction between Q and non Q wave infarction need not influence management decisions in patients after myocardial infarction.
Pre-discharge exercise tests were performed in 359 survivors of an acute myocardial infarction to determine the frequency, characteristics and prognostic implications of silent ischaemia. Tests were negative in 152 patients (42%), silent ischaemia was observed in 103 (29%) and painful ischaemia in 82 (23%). Heart rates at the development of ischaemia and the final double products were similar in both ischaemic groups but patients with silent ischaemia were able to exercise for longer (13.1 +/- 0.5 min) than those with painful ischaemia (9.3 +/- 0.5 min; P less than 0.0001). The 12 month mortality rose from 2% in patients with a negative test, to 4% in those with silent ischaemia and to 8% in those with painful ischaemia. Re-infarction rates increased similarly across the groups (3%, 8% and 18% respectively). Patients with silent ischaemia subsequently developed angina more frequently (47%) than those with negative tests (16%; P less than 0.001). These results suggest that exercise-induced silent ischaemia following myocardial infarction was common, occurring in 29% of patients. Although the final myocardial oxygen consumption was similar in both ischaemic groups those with silent ischaemia were able to exercise for longer. Finally silent ischaemia conferred an intermediate risk of death or re-infarction and was a strong predictor of subsequent angina pectoris.
Basal venous blood levels of several components of the fibrinolytic enzyme system (plasminogen activator, plasminogen, fibrin degradation products, alpha 2-antiplasmin, and alpha 2-macroglobulin) were measured in 100 white men with angiographically defined coronary artery disease. The tests of fibrinolysis were not related to the severity of coronary artery disease, as indicated either by the number of vessels involved or by a coronary score system. Fibrinogen levels, however, did show a modest association with the extent of coronary atheroma (r = 0.21, p less than 0.05). Triglyceride levels were associated with the inhibitors of fibrinolysis: positively with alpha 2-antiplasmin (r = 0.31, p less than 0.005) and negatively with alpha 2-macroglobulin (r = -0.25, p less than 0.05). The alpha 2-antiplasmin levels were significantly elevated in patients with hypertriglyceridaemia. Neither smoking nor beta-blockade had any effect on the tests of fibrinolysis. This study adds support to the association of plasma fibrinogen with ischaemic heart disease.
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A randomised double-blind parallel group study was performed to compare the clinical efficacy of bepridil, a new calcium slow channel blocker, with that of propranolol and placebo in patients with chronic stable angina of effort. Efficacy was assessed objectively by dynamic exercise testing using an upright bicycle ergometer and subjectively by patient documentation of anginal frequency and nitrate consumption. The administration of bepridil resulted in a significant improvement in physical work capacity expressed as calculated maximal oxygen uptake (Vo2 max) and exercise time. This was associated with subjective improvement in terms of reduced anginal frequency. Despite baseline differences in exercise performance and anginal frequency between the three treatment groups, the beneficial effects of bepridil were statistically significant when compared to propranolol. Although minor electrocardiographic changes were noted, no adverse effects were evident when bepridil was prescribed in doses of up to 400 mg/day over a 10 week period.
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Elevated oestradiol (E2) levels may be a risk factor for ischaemic heart disease in men, although the mechanisms for the elevation of oestrogen and for its adverse effects remain unclear. We have studied 100 Caucasian males undergoing elective coronary angiography for ischaemic chest pain and measured serum oestradiol, a profile of haemostatic tests, extent of coronary artery disease and evidence of previous myocardial infarction in order to assess any relationships which could explain the effect of elevated serum oestradiol levels. Levels were significantly higher in men with a history of myocardial infarction compared to those without (p less than 0.01), but were unrelated to the extent of coronary disease or to the haemostatic tests. These results suggest that the association of oestradiol with coronary events relates to myocardial infarction, not to atherogenesis, and is not due to any currently measurable alterations of haemostasis. Current beta-adrenoceptor blocker treatment was associated with lower oestradiol and thromboxane B2 concentrations (both, p = 0.06). These incidental findings suggest that further studies of the effects of beta-blockade on oestradiol and thromboxane metabolism are indicated.
Torsade de pointes is an uncommon ventricular tachyarrhythmia precipitated by a variety of metabolic and pharmacological conditions and requiring unconventional antiarrhythmic therapy. A case is presented demonstrating the occurrence of torsade de pointes following sotalol overdosage and specific features enabling recognition and treatment of this life-threatening arrhythmia are discussed.
The immediate therapy of severe left ventricular (LV) failure after acute myocardial infarction (AMI) frequently requires simultaneous preload reduction, pump output augmentation, and maintenance of systemic blood pressure. Therefore the effects of intravenous nitroglycerin (NG) and dobutamine (DB) were evaluated in 12 patients with severe LV failure following AMI. Nitroglycerin achieved salutary lowering of abnormally elevated LV filling pressure (23 to 14 mm Hg, p less than 0.001) while DB markedly augmented LV pump function (cardiac index rose from 1.7 to 2.5 L/min/m2, p less than 0.005). Notably, the combined infusion of NG + DB simultaneously decreased preload (LV filling pressure 23 to 14 mm Hg, p less than 0.001) and markedly enhanced LV pump performance (cardiac index increased from 1.7 to 2.4 L/min/m2, p less than 0.001). Minor decline in mean systemic blood pressure with NG (72 to 66 mm Hg, p less than 0.05) was rapidly reversed by DB addition (69 mm Hg, p greater than 0.05). Both agents were well tolerated without clinical or ECG evidence of myocardial ischemia or dysrhythmias. Thus the principally venodilator effects of NG minimize systemic hypotension while salutary augmentation of cardiac function in AMI with LV failure is achieved by NG + DB.
The cardiocirculatory actions of the oral vasodilator prazosin were evaluated by cardiac catheterization, forearm plethysmography, echocardiography, treadmill exercise, and symptoms in patients with advanced long-standing congestive heart failure. The administration of oral prazosin (2-7mg) reduced forearm venous tone and forearm vascular resistance. Concomitantly, mean systemic arterial pressure and left ventricular filling pressure decreased, and the cardiac index increased. These effects of a single dose of prazosin on left ventricular function were rapid in onset, maximal at 1 h, and sustained for the entire 6-h period of observation. After 2 weeks of outpatient therapy with 2-7 mg of prazosin four times daily, echographic end-diastolic dimension decreased, whereas the duration of treadmill exercise increased. Symptoms (dyspnea, fatigue, angina) were diminished throughout the course of prazosin therapy, and there was an improvement in the New York Heart Association functional class from 3.7 to 2.2. Thus, prazosin possesses sustained nitroprusside-like balanced dilator actions on the systemic arterial and venous beds, which are effectively translated into the beneficial hemodynamic effects of augmenting cardiac output and relieving excessive left ventricular end-diastolic pressure. The delayed vasodilator tolerance that occurs in 30% of the patients is prevented by the prior use of aldosterone antagonists, and is easily treated when present. Subacute hemodynamic suppression of beneficial prazosin vasodilator actions is transient and does not preclude successful sustained prazosin therapy of severe heart failure.
The cardiocirculatory actions of brief (69 +/- 5 minutes) infusions of prostaglandin E1 were evaluated in nine chronic coronary heart disease patients with severe left ventricular (LV) failure caused by previous myocardial infarction. Prostaglandin E1 infusion did not alter heart rate (HR) and produced modest declines in mean systemic blood pressure (BP) (85 +/- 6 to 76 +/- 5 mm Hg, P less than 0.025) and LV filling pressure (19 +/- 3 to 15 +/- 2 mm Hg, P less than 0.01). Simultaneously, prostaglandin E1 augmented LV pump function raising cardiac index from 1.9 +/- 0.2 to 2.5 +/- 0.1 L/min/m2 (p less than 0.005), elevating stroke index from 28 +/- 2.4 to 35 +/- 2.9 ml/beat/m2 (p less than 0.01), and increasing stroke work index from 26 +/- 4.3 to 30 +/- 4.4 gm . m/m2 (p less than 0.02). Additionally, total systemic vascular resistance decreased from 1862 +/- 192 to 1282 +/- 100 dynes-sec-cm-5 (p less than 0.02) and double product LV aerobic index of HR . systolic BP diminished from 9492 +/- 666 to 8278 +/- 492 (p less than 0.02). Concomitantly, in the forearm, vascular resistance fell, blood flow rose, and venous tone remained unchanged. These results indicate that prostaglandin E1 is a potent systemic arteriolar dilator with markedly beneficial effects on cardiac function in chronic coronary patients having severe ischemic LV failure refractory to conventional therapy.