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Australian Journal of Pharmacy : November 2006
cdi: drug news • approved CPE pharmacy ed u Risk of excessive lowering of blood pressure I T has been suggested that because coronary perfusion occurs mainly during diastole, patients with coronary artery disease (CAD) could be at increased risk for coronary events if diastolic pressure falls below critical levels.1 A study has been carried out to determine whether low blood pressure could be associated with excess mortality and morbidity in patients with CAD.1 The study consisted of a secondary analysis of data from the International Verapamil-Trandolapril Study (INVEST).2 The objective of the INVEST study was to compare mortality and morbidity outcomes in patients with hypertension and CAD treated with verapamil [sustained release] plus trandolapril (a calcium antagonist strategy) or atenolol plus hydrochlorothia- zide (a non-calcium antagonist strategy). The study was a randomised, open label, blinded end point one of 22 576-hypertensive CAD patients aged 50 years or older, which was conducted September 1997 to February 2003 at 862 sites in 14 countries. It was concluded from the data: ‘The verapamil–trandolapril- based strategy was as clinically effective as the atenolol– hydrochlorothiazide-based strategy in hypertensive CAD patients.’ The data collected in the INVEST study was re-examined to evaluate the relationship between average on-treatment blood pressure and risk for the primary outcome (all-cause death, nonfatal stroke, and nonfatal myocardial infarction [MI]), all- cause death, total MI, and total stroke. It was found that the relationship between blood pressure and the primary outcome, all-cause death, and total MI was J- shaped, particularly for diastolic pressure, with a nadir at 119/84mmHg. The best outcomes were seen with a diastolic blood pressure between 80mmHg and 90mmHg. A diastolic blood pressure between 70mmHg and 80mmHg was associated with slightly, but not significantly, worse outcomes. Patients with blood pressures of lower than 70mmHg experienced bad outcomes at the same rate as those with readings higher than 100mmHg. It was concluded: ‘The risk for the primary outcome, all-cause death, and MI, but not stroke, progressively increased with low diastolic blood pressure. Excessive reduction in diastolic pressure should be avoided in patients with CAD who are being treated for hypertension.’ It has been pointed out: ‘The study examined associations between blood pressure and outcomes; it could not prove that the antihypertensive therapy that lowered diastolic pressure ‘too much’ caused the adverse outcomes.’1 1. FH Messerli, G Mancia, CR Conti, et al. Dogma disputed: can aggressively lowering blood pressure in hypertensive patients with coronary artery disease be dangerous? Annals of Internal Medicine 2006;144: 884–893. 2. CJ. Pepine, EM. Handberg, RM. Cooper-DeHoff, et al. A calcium antagonist vs a non-calcium antagonist hypertension treatment strategy for patients with coronary artery disease: the international verapamil-trandolapril study (INVEST): A Randomized Controlled Trial. JAMA. 2003;290:2805–2816. ¦ High-dose statin use reduces the risk of further stroke I T is well established that statins reduce the incidence of strokes among patients at increased risk for cardiovascular disease. However, it is not known whether they reduce the risk of stroke after a recent stroke or transient ischaemic attack (TIA). The stroke prevention by aggressive reduction in cholesterol levels (SPARCL) trial has been carried out to investigate this.1 Some 4,731 patients who had had a stroke or TIA within one to six months before study entry, had low-density lipoprotein (LDL) cholesterol levels of 100 to 190mg per decilitre (2.6 to 4.9mmol per litre), and had no known coronary heart disease (CHD) were involved in the study. They were randomly assigned to receive either atorvastatin (80mg daily)2 or placebo. The trial was carried out double blind and the primary end point was a first nonfatal or fatal stroke during a median follow- up period of 4.9 years. It was found that: • The mean LDL cholesterol level during the trial was 73mg per decilitre among patients receiving atorvastatin and 129mg per decilitre among patients receiving placebo. • 265 patients (11.2 per cent) receiving atorvastatin and 311 patients (13.1 per cent) receiving placebo had a fatal or non- 80 ? THE AUSTRALIAN JOURNAL OF PHARMACY, VOL.87 NOVEMBER 2006 fatal stroke (five-year absolute reduction in risk, 2.2 per cent). • The atorvastatin group had 218 ischaemic strokes and 55 haemorrhagic strokes, whereas the placebo group had 274 ischaemic strokes and 33 haemorrhagic strokes. • The five-year absolute reduction in the risk of major cardio- vascular events was 3.5 per cent (hazard ratio, 0.80). • The overall mortality rate was similar, with 216 deaths in the atorvastatin group and 211 deaths in the placebo group (P=0.98), as were the rates of serious adverse events. • Elevated liver enzyme values were more common in patients taking atorvastatin. It was concluded: ‘In patients with recent stroke or TIA and without known CHD, 80mg of atorvastatin per day reduced the overall incidence of strokes and of cardiovascular events, despite a small increase in the incidence of haemorrhagic stroke.’ 1. Amarenco P, Bogousslavsky J, Callahan A, et al. High-dose atorvastatin after stroke or transient Ischaemic attack. NEJM 2006;355:549–559. 2. The approved dosage range of Lipitor in Australia is 10–80mg/day as a single daily dose. ¦