Traditional risk factors and lifetime risk of acute coronary events

Objective: To investigate the association between the four traditional coronary heart disease (CHD) risk factors (hypertension, smoking, hypercholesterolemia, and diabetes) and outcomes of first ACS. Methods: Data were drawn from the ISACS Archives. The study participants consisted of 70953 patients with first ACS, but without prior CHD. Primary outcomes were patient’ age at hospital presentation and 30-day all-cause mortality. The risk ratios for mortality among subgroups were calculated using a balancing strategy by inverse probability weighting. Trends were evaluated by Pearson's correlation coefficient (r). Results: For fatal ACS (n=6097), exposure to at least one traditional CHD-risk factor ranged from 77.6% in women to 74.5% in men. The presence of all four CHD-risk factors significantly decreased the age at time of ACS event and death by nearly half a decade compared with the absence of any traditional risk factors in both women (from 67.1±12.0 to 61.9±10.3 years; r=-0.089, P<0.001) and men (from 62.8±12.2 to 58.9±9.9 years; r=-0.096, P<0.001). By contrast, there was an inverse association between the number of traditional CHD-risk factors and 30-day mortality. The mortality rates in women ranged from 7.7% with four traditional CHD-risk factors to 16.3% with no traditional risk factors (r=0.073, P<0.001). The corresponding rates in men were 4.8% and 11.5% (r=0.078, P<0.001), respectively. The risk ratios among individuals with at least one CHD-risk factors vs. those with no traditional risk factors were 0.72 (95%CI:0.65-0.79) in women and 0.64 (95%CI:0.59-0.70) in men. This association was consistent among patient subgroups managed with guideline-recommended therapeutic options. Conclusions: The vast majority of patients who die for ACS have traditional CHD-risk factor exposure. Patients with CHD-risk factors die much earlier in life, but they have a lower relative risk of 30-day mortality than those with no traditional CHD-risk factors, even in the context of equitable evidence‐based treatments after hospital admission.

Regulation of wake-sleep states and state-dependent cardiovascular function in diet-induced obesity rats

Obesity often predisposes to coronary heart disease, heart failure, and sudden death. Also, several studies suggest a reciprocal enhancing interaction between obesity and sleep curtailment. Aim of the present study was to go deeper in the understanding of sleep and cardiovascular regulation in an animal model of diet-induced obesity (DIO). According to this, Wake-Sleep (W-S) regulation, and W-S dependent regulation of cardiovascular and metabolic/thermoregulatory function was studied in DIO rats, under normal laboratory conditions and during sleep deprivation and the following recovery period, enhancing either wake or sleep, respectively. After 8 weeks of the delivery of a hypercaloric (HC) diet, treated animals were heavier than those fed a normocaloric (NC) diet (NC: 441 ±17g; HC: 557±17g). HC rats slept more than NC ones during the activity period (Dark) of the normal 12h:12h light-dark (LD) cycle (Wake: 67.3±1.2% and 57.2 ±1.6%; NREM sleep (NREMS): 26.8±1.0% and 34.0±1.4%; REM sleep (REMS): 5.7±0. 6% and 8.6±0.7%; for NC and HC, respectively; p<0.05 for all). HC rats were hypertensive throughout the W-S states, as shown by the mean arterial blood pressure values across the 24-h period (Wake: 90.0±5.3 and 97.3±1.3; NREMS: 85.1±5.5 and 92.2±1.2; REMS: 87.2±4.5 and 96.5±1.1, mmHg for NC and HC, respectively; p<0.05 for all). Also, HC rats appeared to be slightly bradycardic compared to NC ones (Wake: 359.8±9.3 and 352.4±7.7; NREMS: 332.5±10.1 and 328.9±5.4; REMS: 338.5±9.3 and 334.4±5.8; bpm for NC and HC, respectively; p<0.05 for Wake). In HC animals, sleep regulation was not apparently altered during the sleep rebound observed in the recovery period following sleep deprivation, although REMS rebound appeared to be quicker in NC animals. In conclusion, these results indicate that in the rat obesity interfere with W-S and cardiovascular regulation and that DIO rats are suitable for further studies aimed at a better understanding of obesity comorbidities.