Objectives 1. To assess the long-term effectiveness of a comprehensive cardiac rehabilitation programme on quality of life and survival in patients with a large spectrum of cardiovascular diseases (myocardial infarction, acute coronary syndrome, percutaneous transluminal coronary angioplasty and coronary artery bypass grafting). 2. To establish the degree of correlation between expected improvement of health-related quality of life and improvement in physical function attributable to rehabilitation in the intervention group, in comparison with similar changes in the conventional care group. Design Randomized, controlled, parallel-group design (intervention/conventional care). Setting Akershus County, southeast of Oslo City, Norway. Participants 500 patients, men and women, aged 40-85 years, who have sustained at least one of the above-mentioned cardiovascular diseases. Interventions 8 weeks of supervised, structured physical training of three periods of 20 min per week, targeting a heart rate of 60-70% of the individual's maximum; home-based physical exercise training with the same basic schedule as in the supervised period; quantification of patients' compliance with the exercise programme by the use of wristwatches, information stored in the watch memory being retrieved once a month during the 3-year follow-up period; and life-style modification with an emphasis on the cessation of smoking and on healthy nutrition and weight control.

Inhibition of the sodium-hydrogen exchanger (NHE) is a powerful experimental tool to inhibit sodium and calcium accumulation within the ischemic myocyte and halt progression of cell ischemia to cell necrosis. This paper describes the protocol and rationale of a first large-scale clinical trial designed to evaluate the safety and efficacy of cariporide, a novel specific and potent inhibitor of the exchanger.

Hypertrophic cardiomyopathy (HCM) is a dominant genetic disorder of the myocardium associated with dysfunctional contractile proteins. The major risk of HCM is sudden cardiac death, which may occur even in asymptomatic carriers. Causes are highly heterogeneous. Over 140 different mutations in nine sarcomeric genes have been described to date. The majority of cases (80% or more) may eventually be traced to one of these genes. Although genetic counselling is suggested even if mutations are not known, molecular diagnosis implies new options such as carrier identification or - theoretically - preclinical risk stratification. A scheme according to which cardiologists and clinical and molecular geneticists could cooperate in counselling patients and managing HCM clinically is proposed.

Biventricular pacing or resynchronisation therapy is a non-pharmacological therapy for patients with chronic heart failure. Since being originally described in 1994, biventricular pacing has become a subject of intense interest and investigation. This review analyses the results reported in observational series and randomised trials, and seeks to answer two questions. If it works, why does it work? Which heart failure patients will it benefit?

The identification of angiogenic growth factors, such as vascular endothelial growth factor and fibroblast growth factor, has fueled interest in using such factors to induce therapeutic angiogenesis. The results of numerous animal studies and clinical trials have offered promise for new treatment strategies for various ischemic diseases. Increased understanding of the cellular and molecular biology of vessel growth has, however, prompted investigators and clinicians alike to reconsider the complexity of therapeutic angiogenesis. The realization that formation of a stable vessel is a complex, multistep process may provide useful insights into the design of the next generation of angiogenesis therapy.

Large scale clinical trials demonstrate significant reductions in cardiovascular event rates with statin therapy. The observed benefit of statin therapy, however, may be larger in these trials than that expected on the basis of lipid lowering alone. Emerging evidence from both clinical trials and basic science studies suggest that statins have anti-inflammatory properties, which may additionally lead to clinical efficacy. Measurement of markers of inflammation such as high sensitivity C-reactive protein in addition to lipid parameters may help identify those patients who will benefit most from statin therapy.

Objective To assess the effects of a 6-month angiotensin-converting enzyme (ACE) inhibitor intervention on myocardial ischaemia. Method We randomized 389 patients with stable coronary artery disease to double-blind treatment with ramipril 5 mg/day (n = 133), ramipril 1.25 mg/day (n = 133), or placebo (n = 123). Forty-eight-hour ambulatory electrocardiography was performed at baseline, and after 1 and 6 months. Results Relevant baseline variables were similar in all groups. Changes over 6 months in duration of ≥ 1 mm ST-segment depression (STD), total ischaemic burden and maximum STD did not differ significantly between the treatment groups. There was no difference in the frequency of adverse events between the groups. Conclusion ACE inhibitor treatment has little impact on incidence and severity of myocardial ischaemia in patients with stable ischaemic heart disease.

Surrogate outcomes are frequently used in cardiovascular disease research. A concern is that changes in surrogate markers may not reflect changes in disease outcomes. Two recent clinical trials (Heart and Estrogen/Progestin Replacement Study [HERS], and the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [ALLHAT]) underscore this problem since their results contradicted what was expected based on the surrogate outcomes. The current regulatory policy to allow new therapies to be introduced onto the market based solely on surrogate outcomes may need to be reviewed.