Vitamin E: No CV Benefit, Possible Harm
Long-term use of the antioxidant vitamin E does not prevent cardiovascular disease, and it may actually raise the risk of heart failure in high-risk patients, reported Eva Lonn, M.D., of McMaster University in Hamilton, Ont., and her associates.
Despite previous studies that reported promising data on vitamin E, Dr. Lonn and her colleagues in the large, international Heart Outcomes Prevention Evaluation (HOPE) study found that vitamin E provided no cardiovascular benefit in patients with known vascular disease or diabetes. They extended the follow-up of that study to determine whether longer-term treatment might show that vitamin E prevents cardiovascular disease. In the extended study, 3,994 subjects took either daily vitamin E (400 IU) or placebo for an average of 7 years. Vitamin E had no effect on rates of MI, stroke, cardiovascular death, unstable angina, revascularization procedures, or total mortality (JAMA 2005;293:1338-47).
“We observed an unexpected and disturbing increase in heart failure rates in patients assigned to vitamin E. Although this finding could be due to chance, several factors persuade us to believe that it may be real,” they said. Patients with vascular disease or diabetes should not use the supplements until more research is done.
Sudden Death in Obstructive Apnea
People with obstructive sleep apnea show a marked rise in the incidence of sudden cardiac death during sleeping hours, a striking contrast to the nighttime nadir in sudden cardiac death seen in the general population, said Apoor S. Gami, M.D., and associates at the Mayo Clinic, Rochester, Minn.
The investigators reviewed the records of Minnesota residents who underwent sleep studies between 1987 and 2003 and identified 112 of these people who had sudden cardiac death during that period. A total of 78 of these patients had obstructive sleep apnea (OSA), and 34 had other sleep disorders or no sleep disorder.
The frequency of sudden cardiac death occurring between midnight and 6 a.m. was much higher in those with OSA (46%) than in the others (21%) and was higher than that reported in the general population (16%) or the frequency that would be expected by chance (25%). In addition, the severity of OSA correlated with the risk of sudden cardiac death during sleep hours; subjects who died during sleep hours had more severe apnea than those who died at other times of day, the investigators said (N. Engl. J. Med. 2005:352:1206-14).
The mean age at sudden cardiac death was the same for those who died during sleep hours and those who died at other times, and the same as that reported for sudden cardiac death in the general population. This suggests that OSA “does not hasten sudden death from cardiac causes.”
Pulmonary Effects of Antihypertensives
The antihypertensive agent celiprolol, a cardioselective β-blocker, produced fewer adverse pulmonary effects than propranolol and metoprolol in a small study of patients with mild to moderate chronic obstructive pulmonary disease, according to Hanneke van der Woude, M.D., of Martini Hospital, Groningen, the Netherlands, and associates.
Although the adverse effects of β-blockers on asthma are well known, their effects on COPD have been unclear. In this randomized trial of 15 patients, forced expiratory volume in 1 second deteriorated only with propranolol treatment, and airway hyperresponsiveness increased with both propranolol and metoprolol. Propranolol also markedly impaired the bronchodilating effect of the rescue agent formoterol. But celiprolol showed none of these adverse effects, the investigators said (Chest 2005;127:818-24).
Oral Tobacco Raises BP, Heart Rate
Chewing tobacco raises blood pressure, heart rate, and plasma epinephrine, which may contribute to intravascular thrombosis and cardiac arrhythmias, reported Robert Wolk, M.D., of the Mayo Clinic, Rochester, Minn., and his associates.
Noting that the cardiovascular effects of smokeless tobacco are not well understood and that more than 5,000,000 adults and 750,000 adolescents use it, the researchers studied the acute effects of smokeless tobacco on 16 healthy men (mean age 21) who were regular users. Heart rate, blood pressure, and plasma epinephrine levels rose significantly after subjects used 3.0 g of chewing tobacco for 30 minutes but did not change when subjects used a placebo snuff (J. Am. Coll. Cardiol. 2005;45:910-4).
Norepinephrine levels and peripheral vascular resistance did not change despite the marked increase in blood pressure. The findings suggest that chewing tobacco is “a powerful autonomic and hemodynamic stimulus,” and that its pressor effect “results most likely from an increase in cardiac output,” the investigators said.