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Aims: We assessed whether a novel programme to evaluate/communicate predicted coronary heart disease (CHD) risk could lower patients' predicted Framingham CHD risk vs. usual care. Methods: The Risk Evaluation and Communication Health Outcomes and Utilization Trial was a prospective, controlled, cluster-randomised trial in nine European countries, among patients at moderate cardiovascular risk. Following baseline assessments, physicians in the intervention group calculated patients' predicted CHD risk and were instructed to advise patients according to a risk evaluation/communication programme. Usual care physicians did not calculate patients' risk and provided usual care only. The primary end-point was Framingham 10-year CHD risk at 6 months with intervention vs. usual care. Results: Of 1103 patients across 100 sites, 524 patients receiving intervention, and 461 receiving usual care, were analysed for efficacy. After 6 months, mean predicted risks were 12.5% with intervention, and 13.7% with usual care [odds ratio = 0.896; p = 0.001, adjusted for risk at baseline (17.2% intervention; 16.9% usual care) and other covariates]. The proportion of patients achieving both blood pressure and low-density lipoprotein cholesterol targets was significantly higher with intervention (25.4%) than usual care (14.1%; p < 0.001), and 29.3% of smokers in the intervention group quit smoking vs. 21.4% of those receiving usual care (p = 0.04). Conclusions: A physician-implemented CHD risk evaluation/communication programme improved patients' modifiable risk factor profile, and lowered predicted CHD risk compared with usual care. By combining this strategy with more intensive treatment to reduce residual modifiable risk, we believe that substantial improvements in cardiovascular disease prevention could be achieved in clinical practice.

Little is known of the attitudes and behaviours of the general public with regard to their general and personal risk factors for coronary heart disease (CHD), particularly in relation to cholesterol. This study attempted to determine patient perceptions of general population and personal risks regarding cardiovascular disease. Face-to-face interviews were conducted with 5104 members of the public in five countries (France, Germany, Italy, Sweden and the UK). Main results showed only 45% of the public correctly identified CHD as the leading cause of death in their country, and only 51% were aware that high cholesterol increases CHD risk. The presence of cardiovascular disease or risk factors in respondents did not appear to alter perceptions of risk compared with the public who had no existing disease. Of the different nationalities interviewed, the Swedes and the Germans appeared to be most aware of CHD risk factors. Awareness and knowledge of LDL-C and HDL-C were very poor in all countries except Italy Half of the general public (50%) reported they had never discussed their cholesterol levels with a physician and only 33% knew what their target level was. Despite this, the most common source of information on CHD and cholesterol was the physician (60%). Only 9% of the total sample reported that they were currently taking medication for high cholesterol, compared with 20% for hypertension. In summary the general public in several European countries has major lack of awareness of the risks of CHD. This gap in knowledge is particularly marked over the risks of high cholesterol. Significant public health education is required.

The importance of the effects of ACE inhibitors on sudden death, progressive heart failure and recurrent infarction to the reduction in overall mortality in heart failure and after myocardial infarction is disputed.The AIRE study randomized 2006 patients with clinical or radiological evidence of heart failure within 2-9 days of a myocardial infarction to receive ramipiril 5 mg b.d. or matching placebo. Outcomes were assessed independently by members of an end-points committee blinded to treatment allocation.Fewer patients developed severe resistant heart failure as their first validated end-point on rampril, despite the greater number of at-risk survivors, compared to placebo (n = 143 vs 178; risk reduction 23%; CI 5 to 39%; P = 0.017). Ramipril did not alter the rate of reinfarction or stroke. Irrespective of treatment allocation 182 (46%) patients developed resistant heart failure prior to death. A validated acute or remote myocardial reinfarction occurred in 76 (19%) patients prior to death and chest pain occurred in 90 (23%) patients around the time of death suggesting an ischaemic element to these deaths Eighty deaths occurred on the index admission, 167 during re-admission and 145 out-of-hospital. Sudden death accounted for 54% of all deaths and 93% of out-of-hospital deaths. Ramipril reduced the risk of sudden death by 30% (95% CI: 8-47%; P = 0.011). However, overall, 45% of those patients who died suddenly had severe or worsening heart failure prior to their death. Only 39% of sudden deaths were considered to be due to arrhythmias. Ramipril reduced the risk of death from circulatory failure by 18%, but this did not reach statistical significance (95% CI; 41 to -14%; P = 0.237). The magnitude of the effects on sudden death and death due to circulatory failure were not significantly different. However, 38% of the reduction in overall mortality was from the subgroup with sudden death who had developed prior severe resistant heart failure (placebo n = 35, ramipril n = 15), again emphasizing the marked benefit in preventing failure. Ramipril did not selectively alter the proportion of in- to out-of-hospital deaths.Ramipril reduces mortality and progression to resistant heart failure among patients with evidence of heart failure early after myocardial infarction. Retarding the progression of heart failure appears to be a major factor contributing to the reduction in mortality both by reducing circulatory failure and by reducing sudden death.

Objectives. Changes in the electrical activity of the heart reflecting the infarct process can be recorded by continuous vector-ECG, a method which is now clinically available for cardiac supervision. Shifts of the ST-segment and QRS-vector reflect ischaemia and necrosis of the myocardium. Continuous vector-ECG changes were evaluated against myocardial scintigraphy in 18 patients with acute myocardial infarction treated with streptokinase in order to study the impact of improved myocardial perfusion. Design. Myocardial perfusion was analysed with 99 Tc m -Sestamibi (Cardiolite, DuPont Scandinavia AB, Kista, Sweden) single photon emission computerized tomography (SPECT). Registrations were performed before and after thrombolysis in order to estimate the amount of myocardium with impaired perfusion initially (threatened myocardium) and the degree of perfusion improvement in this myocardial area. X, Y, Z vectors were registered continuously by Frank leads (Ortivus Medical, Taby, Sweden). QRS-vector difference, and the time to plateau phase and the ST-vector magnitude were used as a measurement of ischaemia and size of the myocardial infarction. Results. In seven out of 11 patients treated within 3h of onset of symptoms, an improvement in myocardial perfusion in the initially hypoperfused areas was achieved in contrast to none of the seven patients treated > 3 h after onset of pain (P < 0.05). In the whole patient material, there was a negative correlation between the time to plateau level for the QRS-vector and the improvement in myocardial perfusion (r = -0. 53, P < 0.05). Among patients treated within 3 h, there was a negative correlation between the plateau level for the QRS-vector magnitude compared to the improvement in myocardial perfusion (r = -0.61, P < 0.05) and a negative correlation between the plateau level and the myocardial perfusion level after therapy (r = -0.69, P < 0.05). In these patients, there were also negative correlations between the maximal ST-vector magnitude and the myocardial perfusion both before and after thrombolysis (r = -0.81, P < 0.05 and r = -61, P < 0.05, respectively). Conclusion. Patients with marked improvement in myocardial perfusion indicating successful thrombolysis reach their plateau levels of the QRS-change faster and have lower total QRS-vector differences than patients without successful thrombolysis as reflected by myocardial scintigraphy. Patients with a high ST-vector magnitude have low perfusion levels both before and after therapy indicating a pronounced ischaemic damage of the myocardium. Thus, VCG-changes reflect impairment in myocardial perfusion during acute myocardial infarction.