Effect of an intervention to improve the cardiovascular health of family members of patients with coronary artery disease: a randomized trial.

BACKGROUND: Family members of patients with coronary artery disease (CAD) have higher risk of vascular events. We conducted a trial to determine if a family heart-health intervention could reduce their risk of CAD. METHODS: We assessed coronary risk factors and randomized 426 family members of patients with CAD to a family heart-health intervention (n = 211) or control (n = 215). The intervention included feedback about risk factors, assistance with goal setting and counselling from health educators for 12 months. Reports were sent to the primary care physicians of patients whose lipid levels and blood pressure exceeded threshold values. All participants received printed materials about smoking cessation, healthy eating, weight management and physical activity; the control group received only these materials. The main outcomes (ratio of total cholesterol to high-density lipoprotein [HDL] cholesterol; physical activity; fruit and vegetable consumption) were assessed at 3 and 12 months. We examined group and time effects using mixed models analyses with the baseline values as covariates. The secondary outcomes were plasma lipid levels (total cholesterol, low-density lipoprotein cholesterol, HDL cholesterol and triglycerides); glucose level; blood pressure; smoking status; waist circumference; body mass index; and the use of blood pressure, lipid-lowering and smoking cessation medications. RESULTS: We found no effect of the intervention on the ratio of total cholesterol to HDL cholesterol. However, participants in the intervention group reported consuming more fruit and vegetables (1.2 servings per day more after 3 mo and 0.8 servings at 12 mo; p < 0.001). There was a significant group by time interaction for physical activity (p = 0.03). At 3 months, those in the intervention group reported 65.8 more minutes of physical activity per week (95% confidence interval [CI] 47.0-84.7 min). At 12 months, participants in the intervention group reported 23.9 more minutes each week (95% CI 3.9-44.0 min). INTERPRETATION: A health educator-led heart-health intervention did not improve the ratio of total cholesterol to HDL cholesterol but did increase reported physical activity and fruit and vegetable consumption among family members of patients with CAD. Hospitalization of a spouse, sibling or parent is an opportunity to improve cardiovascular health among other family members. TRIAL REGISTRATION: clinicaltrials.gov, no NCT00552591.

Impact of program duration and contact frequency on efficacy and cost of cardiac rehabilitation: results of a randomized trial.

BACKGROUND: Secondary prevention through cardiac rehabilitation (CR) has been recommended for most patients with coronary artery disease (CAD). Although generally reimbursed for 3 months, to date, optimal CR program duration and frequency of patient contact has yet to be identified. This study compared standard (33 sessions for 3 months) versus distributed (33 sessions for 12 months) CR for effects on exercise variables, risk factors, health-related quality of life (HRQL), depressive symptoms, and direct costs to the cardiac health care system. METHODS: We randomly assigned 392 patients to either standard CR (n = 196) or distributed CR (n = 196). Outcomes were cardiorespiratory fitness, daily physical activity, coronary risk factors, generic and heart disease HRQL, and depressive symptoms, measured 12 and 24 months after program intake. Secondary outcomes included these variables measured after 3 months. Costs to the cardiac health care system were determined 2 years after program initiation. RESULTS: Both groups showed improvements over time in cardiorespiratory fitness, daily physical activity, low-density lipoprotein cholesterol, generic and heart disease HRQL, and depressive symptoms. Over time, blood pressure and body mass index values worsened. Smoking status, high-density lipoprotein cholesterol, and triglyceride levels remained unchanged. There were no clinically meaningful or statistically significant between group differences for outcomes at 12 or 24 months. The costs of the programs to the cardiac health care system were not different. CONCLUSIONS: From a clinical standpoint, this study indicates that both standard and distributed program formats serve patients with CAD equally well over the longer term. Programs could use either program delivery model (standard or distributed) depending on patient or program needs. Costs to the cardiac health care system are similar.

Variability in estimating eccentric contraction-induced muscle damage and inflammation in humans.

We studied five young healthy volunteers who performed a "damage protocol" consisting of 240 (24 sets x 10 repetitions/set) maximal isokinetic eccentric muscle contractions (30 degrees/s) on each leg one week apart. Biopsies were taken from the vastus lateralis on two occasions. Two biopsies were taken from within the same muscle 24h following the damage protocol. On a second occasion a single biopsy was taken from the contralateral leg at 24h following the same damage protocol. Biopsies at all three sites showed Z-band disruption, much greater (i.e., approximately 14-fold) than is typically observed in resting biopsies, with no significant differences (ANOVA) according to site location (within legs or between legs). The within-leg coefficient of variation (CV) was, however, 41 +/- 30%, and the between-leg CVs were 57 +/- 36% and 68 +/- 36%. Macrophage cells were also detected within the muscle, and cell numbers were not statistically different between biopsy sites. However, the within-biopsy CV = 52 +/- 19% and the between-biopsy CVs of 34 +/- 24% and 48 +/- 27%. We conclude that eccentric contraction-induced Z-band streaming and inflammatory cell response, as detected in muscle biopsy samples from humans, is highly variable with a CV of 40-70%.

Contraction-induced muscle damage in humans following calcium channel blocker administration.

Following contraction-induced damage of skeletal muscle there is a loss of calcium homeostasis. Attenuating the damage-induced rise in myocellular calcium concentration may reduce proteolytic activation and attenuate other indices of damage; calcium channel blockers have been shown to be effective in this regard. The effect of administration of a calcium channel blocker (CCB), amlodipine, on indices of muscle damage following a unilateral 'damage protocol', during which subjects performed 300 maximal isokinetic (0.52 rad s(-1)) eccentric contractions with the knee extensors was investigated. The design was a randomized, double-blind crossover. On one occasion, prior to the damage protocol, subjects consumed CCB for 7 days prior to and for 7 days following the damage protocol. Biopsies were taken from the vastus lateralis prior to (baseline) and following the damage protocol at 4 h and 24 h post-damage. Isometric peak knee extensor torque was reduced (P < 0.05) immediately post-, 24 h post- and 48 h post-damage protocol compared to pre-exercise values with no effect of treatment. Desmin disruption was attenuated (P < 0.05) with CCB versus placebo at 4 h post-damage. Z-band streaming was significantly (P < 0.05) elevated compared to baseline at both times post-damage, but was lower with CCB at 4 h (P < 0.05). Damage resulted in increased inflammatory cell (macrophage) infiltration into skeletal muscle at both 4 h and 24 h post-damage, with no effect of CCB. Neutrophil number was elevated by the damage protocol, but was higher at 24 h post-damage in the CCB condition (P < 0.05). Creatine kinase (CK) activity was higher (P < 0.05) at 24 h and 48 h following the damage protocol compared to baseline, with no effect of treatment. In conclusion, the reduction in desmin disruption and Z-band streaming indicates that CCB attenuated, or delayed, the contraction-induced damage to sarcomeric proteins.

Contraction-induced muscle damage is unaffected by vitamin E supplementation.

PURPOSE: Vitamin E supplementation may confer a protective effect against eccentrically biased exercise-induced muscle damage through stabilization of the cell membrane and possibly via inhibition of free radical formation. Evidence supporting a protective role of vitamin E after contraction-induced muscle injury in humans is, however, inconsistent. The present study sought to determine the effect of vitamin E supplementation on indices of exercise-induced muscle damage and the postexercise inflammatory response after performance of repeated eccentric muscle contractions. METHODS: Young healthy men performed a bout of 240 maximal isokinetic eccentric muscle contractions (0.52 rad.s-1) after being supplemented for 30 d with either vitamin E (N = 9; 1200 IU.d-1) or placebo (N = 7; safflower oil). RESULTS: Measurements of torque (isometric and concentric) decreased (P < 0.05) below preexercise values immediately post- and at 48 h post-exercise. Biopsies taken 24 h postexercise showed a significant increase in the amount of extensive Z-band disruption (P < 0.01); however, neither the torque deficit nor the extent of Z-band disruption were affected by vitamin E. Exercise resulted in increased macrophage cell infiltration (P = 0.05) into muscle, which was also unaffected by vitamin E. Serum CK also increased as a result of the exercise (P < 0.05) with no effect of vitamin E. CONCLUSION: We conclude that vitamin E supplementation (30 d at 1200 IU.d-1), which resulted in a 2.8-fold higher serum vitamin E concentration (P < 0.01), had no affect on indices of contraction-induced muscle damage nor inflammation (macrophage infiltration) as a result of eccentrically biased muscle contractions.