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Biomedical subjects

J G Cleland

Publications and source records attributed to J G Cleland.

At least 19 recordsLinked to original sources
PubMed1998

Management strategies for a better outcome in unstable coronary artery disease.

Unstable coronary artery disease is a term encompassing both unstable angina and non-Q-wave (non-ST-segment elevation) myocardial infarction. Patients with these conditions are at risk of early progression to acute myocardial infarction and death. Thus, management of these conditions must aim to reduce long-term mortality and morbidity. Risk stratification is crucial for the identification of patients whose risk of early progression is high; they may require coronary angiography and (if suitable) either percutaneous transluminal coronary angioplasty or coronary artery bypass surgery. No single variable can accurately predict risk, but considerable data are emerging to show that biochemical markers of myocardial injury, such as troponin-T and troponin-I, are valuable in combination with electrocardiographic findings and clinical features. Routine early invasive procedures (coronary angiography with or without revascularization) have not yet been shown to have any significant advantage over conservative regimens for the majority of patients. Antiplatelet, anticoagulant, and anti-ischemic agents remain the mainstay of treatment in the acute phase. New agents, such as glycoprotein IIb/IIIa receptor inhibitors and low-molecular-weight heparins, as well as antithrombins and Factor Xa inhibitors add to the treatments currently available. Thrombolytic agents are contraindicated in the absence of ST-segment elevation. After clinical stabilization, ongoing assessment should include exercise testing for all patients who are able; other imaging techniques should be used for patients unable to exercise. A profile indicating a high risk of future events is an indication for elective angiography and consideration for revascularization.

Algorithms↗
PubMed1998

Endothelin-1 has haemodynamic effects at pathophysiological concentrations in patients with left ventricular dysfunction.

OBJECTIVES: Plasma levels of immunoreactive endothelin-1 (ET-1) are raised in chronic heart failure. Whether plasma ET-1 contributes to the haemodynamic derangement found in chronic heart failure is not known. We investigated the effects of exogenous ET-1 on the pulmonary and systemic vasculature in patients with left ventricular systolic dysfunction (LVD), with or without overt heart failure. METHODS: ET-1 was infused at 1, 5 and 15 pmol/min into a distal pulmonary artery of ten patients with LVD to achieve plasma concentrations of ET-1 similar to those found in patients with heart failure and pulmonary hypertension. Haemodynamics were measured using a pulmonary thermodilution catheter and an arterial line. Intravascular Doppler and local pulmonary angiography were used to assess local pulmonary blood flow in the first four patients. RESULTS: Systemic haemodynamic changes occurred with ET-1 infusion: mean arterial pressure (100 +/- 3 [standard error of the mean]) to 107 +/- 3 mmHg; p < 0.01) and systemic vascular resistance (1699 +/- 118 to 2033 +/- 135 dynes s/cm5; p < 0.001) rose, while the cardiac index fell from 2.43 +/- 0.17 to 2.20 +/- 0.16 l/min/m2 (p < 0.002). Mean pulmonary artery pressure (21 +/- 2 mmHg) and pulmonary vascular resistance (151 +/- 14 to 147 +/- 14 dynes s/cm5) did not change however. CONCLUSIONS: Exogenous ET-1, when infused to achieve plasma concentrations similar to those in severe heart failure and pulmonary hypertension, causes systemic but not pulmonary vasoconstriction.

Aged↗
PubMed1998

Etiology and response to drug treatment in heart failure.

Clinical trials in heart failure (HF) tend to randomize patients according to demographic characteristics and severity of left ventricular dysfunction, without taking account of the precise diagnosis. This article reviews results from recent trials suggesting that the etiology of HF, and particularly whether it is ischemic or nonischemic, may influence the long-term prognosis and the response to treatment. Some studies, but not all, suggest that nonischemic HF has a better prognosis than ischemic HF. The data on the benefits of angiotensin-converting enzyme inhibitors in ischemic versus nonischemic HF are conflicting. Carvedilol, and recently, bisoprolol have been shown to reduce mortality in ischemic and nonischemic HF, whereas metoprolol has, to date, improved prognosis only in dilated cardiomyopathy. Better responses to digoxin, amlodipine and amiodarone have been reported in non-ischemic HF. There is at present no clear explanation for the apparent therapeutic differences between ischemic and nonischemic HF. Absence of a rigorous definition of "nonischemic HF" in many studies makes interpretation of the results difficult. Further studies to clarify the effects of etiology of HF on the response to treatment could be particularly important for preventing progression to more advanced stages, in which any type of drug therapy may have limited value in prolonging survival. An individualized therapeutic approach, based on etiology of HF and possibly other factors such as plasma drug levels or the levels of neurohormones, could result in major progress in treating HF patients.

Adrenergic beta-Antagonists↗
PubMed1998

Regional differences in the characteristics and treatment of patients participating in an international heart failure trial. The Assessment of Treatment with Lisinopril and Survival (ATLAS) Trial Investigators.

AIMS: This study was designed to determine regional differences in patient characteristics and medication use among patients entered into an international heart failure trial. METHODS AND RESULTS: Data for this analysis were derived from the Assessment of Treatment with Lisinopril and Survival Study (ATLAS), a prospective randomized comparison of high- and low-dose therapy with lisinopril in patients with New York Heart Association class II, III, or IV chronic heart failure, which enrolled 3164 patients in 291 centers in 19 countries on 3 continents. Information was collected at baseline concerning patient demographics, etiology of heart failure, accompanying conditions, prior revascularization procedures, and medication use. The primary findings were a lower incidence of ischemic cardiomyopathy in southern and western Europe, more frequent diabetes in North America, and a greater use of coronary revascularization in the United States and Canada. There was substantial variation in medication use, particularly with regard to digoxin, anticoagulants, and amiodarone. CONCLUSIONS: Although there is considerable overlap in guidelines concerning the treatment of heart failure issued by authorities in Europe and North America, there are significant regional variations in medication use. Some, but not all, of these differences can be explained by differences in patient characteristics.

Aged↗
PubMed1998

Therapeutic options and cost considerations in the treatment of ischemic heart disease.

Ischemic heart disease is a serious health problem because it causes considerable mortality and morbidity. Given the limited resources for health care, it is important to establish the costs associated with the benefits of its various treatment options. We therefore assessed the costs and benefits of medical treatment versus revascularization in a hypothetical cohort of 100 patients. A spreadsheet model was constructed using published data. The main outputs of this model were health-service costs per year and quality-adjusted survival estimates. In the United Kingdom, costs for treatments of less than 5,000 Pounds/quality-adjusted life-year (QALY) are perceived as highly cost effective, whereas those over 10,000 Pounds/QALY are considered expensive. For patients with intractable symptoms, surgery is highly effective and has benefits on prognosis. In patients with well-controlled symptoms on medical therapy, the benefits of surgery are small and uncertain, and therefore medical therapy is the most cost-effective treatment. Overall, the preferred cost-effective option favored medical treatment.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Should we screen for asymptomatic left ventricular dysfunction to prevent heart failure?

A programme to detect and treat asymptomatic left ventricular dysfunction would seem to fulfil all five principles of screening. Indeed, such a programme would appear to be at least as firmly based as those already in existence for, for example, cervical and breast cancer. Further evaluation of the screening of high risk groups to detect asymptomatic left ventricular systolic dysfunction with the aim of giving treatment to prevent the development of heart failure is merited.

Clinical Trials as Topic↗
PubMed1998

Pulmonary and systemic responses to exogenous endothelin-1 in patients with left ventricular dysfunction.

Plasma levels of immunoreactive endothelin-1 (ET-1) are elevated in chronic heart failure (CHF) and have been reported to correlate closely with pulmonary hemodynamic measurements. We investigated the effects of exogenous ET-1 on the pulmonary vasculature in patients with left ventricular systolic dysfunction (LVD), with or without overt heart failure. ET-1 was infused at 1, 5, and 15 pmol/min into a distal pulmonary artery of 10 patients with LVD. Hemodynamics were measured by a thermodilution catheter and arterial line. Intravascular Doppler and local pulmonary angiography were used to assess local pulmonary blood flow in the first four patients. Systemic hemodynamic changes occurred with ET-1 infusion in a dose-dependent fashion. Mean arterial pressure (100 +/- 8-107 +/- 11 mm Hg; p < 0.01) and systemic vascular resistance (1,699 +/- 375-2,033 +/- 427 dynes/s/cm-5; p < 0.001) rose, whereas the cardiac index fell from 2.43 +/- 0.53 to 2.20 +/- 0.491/min/m2 (p < 0.002). However, mean pulmonary artery pressure (21 +/- 7 mm Hg) and pulmonary vascular resistance (151 +/- 43-147 +/- 43 dynes/s/cm-5) did not change. Exogenous ET-1, when infused into patients with LVD, causes systemic but not pulmonary vasoconstriction.

Aged↗
PubMed1998

Beta-blockers for chronic heart failure: from prejudice to enlightenment.

Experience accumulated from several large trials strongly suggest that beta-blockers should be used for the management of congestive heart failure (CHF). Beta-blockade should be added to conventional therapy such as diuretics, ACE inhibitors, and digoxin, as this was the approach used in the major trials. It is appropriate to treat patients with mild, moderate and, when stable, severe CHF. The benefits obtained include improvements in left ventricular function, reductions in symptoms and morbidity, improvement of quality of life, and delay of clinical progression, reflected by a reduced need for hospitalization and a reduction in mortality. Beta-blockers are much better tolerated, when used appropriately in selected patients, than was previously supposed.

Adrenergic beta-Antagonists↗
PubMed1998

Influence of concomitant disease on patterns of hospitalization in patients with heart failure discharged from Scottish hospitals in 1995.

AIMS: To determine the prevalence of common, serious, concomitant conditions complicating admissions with heart failure and how such conditions influence the length of hospital stay. METHODS AND RESULTS: Data from Scottish morbidity records (SMR1) were used to determine the rate of deaths and discharges for heart failure (ICD-9 428.0, 428.9), concomitant discharge diagnoses and length of stay in 1995. 27,477 SMR1 records listing heart failure as a diagnosis were identified with heart failure in the first position in 11,560 (42%) records. 63.3% of deaths or discharges results from emergency admission. 13.2% of admissions were associated with acute myocardial infarction, 7.3% with angina or chest pain, 11.8% with chronic airways obstruction, 8.3% with chronic or acute renal failure and 5.3% had had a stroke. Length of stay including those patients who died was 7.6 days when acute myocardial infarction was the principal diagnosis but 26.3 days when stroke was the principal diagnosis. CONCLUSION: A large proportion of deaths and discharges for heart failure are associated with conditions other than heart failure that may precipitate, contribute to or complicate admission. Treatment for heart failure that does not also seek to reduce the risk associated with common concomitant diseases may miss opportunities to reduce the overall risk of hospitalization.

Adult↗