European Journal of Preventive Cardiology

Globally hypertension is stabilising, but in sub-Saharan Africa the incidence of hypertension remains on an increase. Although this might be attributed to poor healthcare and ineffective antihypertensive treatment, there is a limited understanding of population and individual-specific cardiovascular pathophysiology – necessary for effective prevention and treatment strategies in Africa. As there is a lack of longitudinal studies tracking the early pathophysiological development of hypertension in black populations, the African-PREDICT study was initiated. The purpose of this paper is to describe the detailed methodology and baseline cohort profile of the study.

From 2013 to 2017, the study included 1202 black (N = 606) and white (N = 596) men and women (aged 20–30 years) from South Africa – screened to be healthy and clinic normotensive. At baseline, and each 5-year follow-up examination, detailed measures of health behaviours, cardiovascular profile and organ damage are taken. Also, comprehensive biological sampling for the ‘omics’ and biomarkers is performed. Overall, the baseline black and white cohort presented with similar ages, clinic and 24-hour blood pressures, but black adults had lower socioeconomic status and higher central systolic blood pressure than white individuals.

The prospective African-PREDICT study in young black and white adults will contribute to a clear understanding of early cardiovascular disease development.

Supervised treadmill exercise for claudication in peripheral arterial disease is effective but poorly tolerated because of ischemic leg pain. Near infrared spectroscopy allows non-invasive detection of muscle ischemia during exercise, allowing for characterization of tissue perfusion and oxygen utilization during training.

We evaluated walking time, muscle blood flow, and muscle mitochondrial capacity in patients with peripheral artery disease after a traditional pain-based walking program and after a muscle oxygen-guided walking program.

Patients with peripheral artery disease trained thrice weekly in 40-minute-long sessions for 12 weeks, randomized to oxygen-guided training (n = 8, age 72 ± 9.7 years, 25% female) versus traditional pain-based training (n = 10, age 71.6 ± 8.8 years, 20% female). Oxygen-guided training intensity was determined by maintaining a 15% reduction in skeletal muscle oxygenation by near infrared spectroscopy rather than relying on symptoms of pain to determine exercise effort. Pain free and maximal walking times were measured with a 12-minute Gardner treadmill test. Gastrocnemius mitochondrial capacity and blood flow were measured using near infrared spectroscopy. Baseline pain-free walking time was similar on a Gardner treadmill test (2.5 ± 0.9 vs. 3.6 ± 1.0 min, p = 0.5). After training, oxygen-guided cohorts improved similar to pain-guided cohorts (pain-free walking time 6.7 ± 0.9 vs. 6.9 ± 1.1 min, p < 0.01 for change from baseline and p = 0.97 between cohorts). Mitochondrial capacity improved in both groups but more so in the pain-guided cohort than in the oxygen-guided cohort (38.8 ± 8.3 vs. 14.0 ± 9.3, p = 0.018). Resting muscle blood flow did not improve significantly in either group with training.

Oxygen-guided exercise training improves claudication comparable to pain-based training regimens. Adaptations in mitochondrial function rather than increases in limb perfusion may account for functional improvement. Increases in mitochondrial oxidative capacity may be proportional to the degree of tissue hypoxia during exercise.

The objective of this study was to evaluate the effect on mortality of self-reported physical activity evaluated by the physical activity scale for the elderly (PASE) in elderly patients with advanced heart failure enrolled in a cardiac rehabilitation unit after heart failure decompensation (NYHA class IIIB).

The study prospectively enrolled 314 elderly patients (≥65 years) with heart failure in NYHA class IIIB (symptomatic with a recent history of dyspnoea at rest) consecutively admitted to cardiac rehabilitation between January 2010 and July 2011. Comprehensive geriatric assessment was performed. Physical activity was evaluated by PASE and stratified in tertiles (0–15, 16–75 and >75). Mortality was collected from September to October 2015 in 300 patients.

The mean age was 74.5 ± 6.1 (range 65–89); 74.7% were men, 132 patients (44.0%) died during the follow-up (44.1 ± 20.7 months). Univariate analysis shows that physical activity level conducted before heart failure decompensation was inversely related to mortality (from 76.0% to 8.2%, P = 0.000). Multivariate analysis confirms that the PASE score predicts mortality independently of several demographic and clinical variables (hazard rate 0.987, 95% confidence interval (CI) 0.980–0.994, P = 0.000). Notably, when considering PASE 0–15 versus 16–75 score and PASE 0–15 versus > 75 score, the hazard rate is 4.06 (95% CI 1.67–9.84, P < 0.001) and 7.25 (95% CI 2.7–19.5, P < 0.001), respectively.

Physical activity level evaluated by the PASE score is inversely related to mortality in elderly patients with advanced heart failure confirming the reduction of mortality exerted by moderate physical activity in such patients.

The respiratory benefits of muscle strength are well-known in heart-healthy populations, but recommendations and research often focus instead on aerobic fitness (peak oxygen uptake) or total activity. Independent benefits of strength thus may be underestimated, especially in congenital heart disease where perceived dangers of certain types of exercise may outweigh perceived benefits. To assess whether it is plausible that pulmonary benefits of strength in heart-healthy populations also apply in congenital heart disease, we simultaneously correlated these patients’ lung function with fitness, strength, and cardiac diagnosis.

Lung function (forced expiratory volume in one second percentage predicted (FEV1%pred)) was modeled as function of handgrip strength, congenital heart disease diagnosis, peak oxygen uptake and the interactions of handgrip with sex and diagnosis in 538 Germans (58% male, ages 6–82 years) in linear models corrected for age, sex, height and weight. Congenital heart disease diagnoses were: complex cyanotic; Fallot/Truncus arteriosus communis (common arterial trunk) (TAC); shunts; transposition of the great arteries (TGA); left heart; and other/none.

Each kg of handgrip was associated with 0.74% higher FEV1%pred (p < 0.001) and handgrip explained almost 10% of variance in FEV1%pred. While some groups had higher FEV1%pred than others (p for global null <0.0001), all experienced similar associations with strength (p for interaction with handgrip >0.10 for both sex and diagnosis.) Correction for peak oxygen uptake eliminated the association with congenital heart disease, but not handgrip.

Strength was associated with better lung function in all ages even after correction for peak oxygen uptake, regardless of sex and congenital heart disease. This suggests that strength may be at least as important for lung function as aerobic fitness. Heart-safe strength training may improve pulmonary function in congenital heart disease.

The purpose of this study was to investigate the risk of rhabdomyolysis in subjects initiating statin therapy for primary prevention of cardiovascular disease, focusing on the type of statin, dose and time since initiation.

A nationwide cohort study using French hospital discharge and claims databases was performed, studying subjects from the general population 40–75 years in 2009, with no history of cardiovascular disease and no lipid-lowering drugs during the preceding three-year period, followed for up to seven years. The primary outcome was hospitalization for rhabdomyolysis. Event-free survival analysis and case-time-control analysis were both performed, separately by gender. The cohort included 8,236,667 subjects, 969,460 of whom initiated a lipid-lowering drug for cardiovascular disease primary prevention. During 18,407,391 person-months exposed to statins, 168 events were observed, corresponding to an incidence of rhabdomyolysis of 1.10 per 10,000 person-years (1.54 in men vs 0.81 in women); 10/168 cases were fatal, and 18/168 and 57/168 cases occurred during the first month and first trimester of treatment, respectively. Survival analysis did not reveal any increased overall risk (hazard ratio = 1.02 (0.83–1.25) in men and 0.76 (0.60–0.96) in women). However, exposure to high-potency statins was associated with an increased risk in men (hazard ratio = 1.93 (1.27–2.94)). Rosuvastatin 20 mg (in men and women) and simvastatin 40 mg (in men) were associated with hazard ratios > 5. Case-time-control analyses showed similar patterns of risk. Drug interactions did not appear to significantly contribute to rhabdomyolysis events in this study.

Although the overall risk of statin-associated rhabdomyolysis in the context of primary prevention was not increased, the first months of treatment and the use of high-potency statins represent at-risk situations, which require appropriate monitoring, especially in men.

Long-term risk factor control after myocardial infarction (MI) is currently inadequate and there is an unmet need for effective secondary prevention programmes.

It was the aim of the study to compare a 12-month intensive prevention programme (IPP), coordinated by prevention assistants and including education sessions, telephone visits and telemetric risk factor control, with usual care after MI. Three hundred and ten patients were randomized to IPP vs. usual care one month after hospital discharge for MI in two German heart centres. Primary study endpoint was the IPP Prevention Score (0–15 points) quantifying global risk factor control.

Global risk factor control was strongly improved directly after MI before the beginning of the randomized study (30% increase IPP Prevention Score). During the 12-month course of the randomized trial the IPP Prevention Score was improved by a further 14.3% in the IPP group (p < 0.001), while it decreased by 11.8% in the usual care group (p < 0.001). IPP significantly reduced smoking, low-density lipoprotein cholesterol, systolic blood pressure and physical inactivity compared with usual care (p < 0.05). Step counters with online documentation were used by the majority of patients (80%). Quality of life was significantly improved by IPP (p < 0.05). The composite endpoint of adverse clinical events was slightly lower in the IPP group during 12 months (13.8% vs. 18.9%, p = 0.25).

A novel intensive prevention programme after MI, coordinated by prevention assistants and using personal teachings and telemetric strategies for 12 months, was significantly superior to usual care in providing sustainable risk factor control and better quality of life.

The effects of increasing high-density lipoprotein cholesterol on cardiovascular outcomes remain uncertain.

We conducted a meta-analysis to investigate the effects of high-density lipoprotein cholesterol modifiers (niacin, fibrates and cholesteryl ester transfer protein inhibitors) on cardiovascular outcomes.

Thirty-one randomized controlled trials (154,601 patients) with a follow-up of 6 months or more and a sample size of 100 or more patients were selected using MEDLINE, EMBASE and CENTRAL database (inception January 2018).

High-density lipoprotein cholesterol modifiers had no statistically significant effect on cardiovascular mortality in terms of relative risk (RR) (RR 0.94, 95% confidence interval (CI) 0.89–1.00, P = 0.05, I² = 13%) or absolute risk (risk difference −0.0001, 95% CI −0.0014, 0.0011, P = 0.84, I² = 28%). High-density lipoprotein cholesterol modifiers reduced the RR of myocardial infarction (RR 0.87, 95% CI 0.82–0.93, P < 0.001, I² = 37%). This significant effect was derived by the use of fibrates (RR 0.80, 95% CI 0.73–0.87, P < 0.001, I² = 22%) and meta-regression analysis showed that this benefit was consistent with an absolute reduction in low-density lipoprotein cholesterol. High-density lipoprotein cholesterol modifiers had no effect on stroke (RR 1.00, 95% CI 0.93–1.09, P = 0.94, I² = 25%) or all-cause mortality (RR 1.02, 95% CI 0.97–1.08, P = 0.48, I² = 49%). Meta-regression analyses failed to demonstrate a significant association of pharmacologically increased high-density lipoprotein cholesterol with key endpoints. In studies with background statin therapy, high-density lipoprotein cholesterol modifiers had no statistically significant impact on cardiovascular mortality, myocardial infarction, stroke or all-cause mortality (P > 0.05).

The use of high-density lipoprotein cholesterol modifying treatments had no significant effect on cardiovascular mortality, stroke or all-cause mortality. The beneficial effect on myocardial infarction was lost when drugs were used with statin therapy.