BACKGROUND: Previous meta-analyses resurrected the debated statement “the lower, the better” following blood pressure (BP)-lowering treatment. We investigated the benefits of BP-lowering treatment at different BP targets by prevention category. METHODS: The meta-analysis protocol was registered at the International Prospective Register of Systematic Reviews (CRD42022379249). The database included 115 BP-lowering or comparison trials from patients with (n=241 089) or without (n=198 937) previous cardiovascular events. Prevention disease groups were stratified by in-treatment achieved BP, drug class versus placebo, and drug class versus other classes. Risk ratios and 95% CIs of major adverse cardiovascular events were calculated. RESULTS: Following a standard (10/5 mm Hg) BP reduction, major adverse cardiovascular event relative risk reductions were not different between prevention groups (primary, 25% [95% CI, 18%–31%]; secondary, 28% [95% CI, 20%–37%]). For achieved systolic BP of at least 140 mm Hg, between 130 and 140 mm Hg, and <130 mm Hg (nadir, 125 mm Hg), (1) risk ratios of major adverse cardiovascular events and absolute risk reductions were not different between prevention groups across systolic BP strata, and (2) residual risk, though 4.1× greater in secondary than primary prevention, decreased in primary prevention from higher to lower systolic BP targets. The effect of separate drugs versus others on the primary outcome was not different between prevention groups. CONCLUSIONS: BP-lowering treatment benefits did not differ by prevention group to a nadir of 125 mm Hg for systolic BP. Although residual risk in secondary prevention is higher than in primary prevention, it gradually decreases at progressively lower systolic BP targets in primary prevention. REGISTRATION: URL: https://www.crd.york.ac.uk/PROSPERO/ ; Unique identifier: CRD42022379249.

Obesity and hypertension have become an international health issue, with detrimental consequences on patients. Obesity and hypertension share common pathophysiological mechanisms, such as overactivity of the renin–angiotensin–aldosterone and the sympathetic nervous systems, insulin resistance, and disruption of the leptin pathway. Approved therapies for obesity and overweight include phentermine/topiramate, orlistat, naltrexone/bupropion, the glucagon-like peptide-1 receptor agonists liraglutide and semaglutide, tirzepatide, and bariatric surgery. This review gives the clinical data in a thorough manner and explains in detail how each of the previously mentioned therapies affects blood pressure levels.

Obesity can cause the onset of heart failure and exacerbate the status of the pre-existing disease. Through intricate pathways, obesity activates hormonal factors that encourage the development of inflammation and lead to increased congestion. Consequently, this complex parallel pathophysiological cascade contributes to the echocardiographic and clinical signs of heart failure. In these patients, obesity frequently coexists with nutritional and muscular profile abnormalities that manifest as cachexia or sarcopenia. Patients with heart failure have a higher chance of surviving when obesity is treated. Interventional, pharmaceutical, and dietary strategies are used as forms of therapy. This review delves into the evaluation of the relationship between obesity and heart failure, and it targets to highlight the therapeutical impact of weight-loss programs on cardiac function in individuals with heart failure and obesity.

BACKGROUND: Sympathetic deactivation represents a major goal of antihypertensive drug treatment. However, whether treatment normalizes the hypertension-related sympathetic cardiovascular overdrive remains uncertain. METHODS: In 219 middle-aged essential hypertensives, we analyzed, along with office systolic and diastolic blood pressure (BP) and heart rate, muscle sympathetic nerve traffic (MSNA, microneurography) before and after 3-month treatment, either as monotherapy or as combination. Controls were represented by 100 age-matched normotensives. RESULTS: Treatment caused, along with a small heart rate decrease, a clear BP reduction (from 160.5/95.5 to 142.3/85.0 mm Hg, P <0.01) and a significant MSNA inhibition (from 70.7±11.5 to 65.0±10.2 bursts/100 heartbeats, mean±SD, P <0.01). A similar pattern was detected in patients under monotherapy (n=81) or combination drug treatment (n=138). MSNA was significantly related to systolic BP before and during treatment but unrelated to heart rate. In treated patients achieving the lower BP (135.1/84.5 mm Hg, n=90), the MSNA reduction was greater than that detected in patients with the higher on-treatment BP (146.7/87.4 mm Hg, n=129). However, even in patients achieving a BP target <140/90 mm Hg, MSNA remained markedly higher (on average +66.4%) compared with controls. This was the case even when treated BP was <130/80 mm Hg. Data were similar for different antihypertensive drug classes. CONCLUSIONS: Thus, antihypertensive treatment, even when effective in achieving BP control, fails to restore the level of normotension-related MSNA, with a persistence of the pattern of heightened sympathetic influences typical of untreated patients with hypertension. Failure of normalization may contribute to the development of the residual cardiovascular risk reported in treated hypertensives.

Anabolic–androgenic steroids (AASs) are synthetic derivatives of testosterone and are increasingly misused to enhance muscle growth and physical performance, particularly among athletes and recreational bodybuilders. Although AASs affect multiple organ systems, their severe and potentially life-threatening complications involve the cardiovascular system. This review summarizes current knowledge on the pathophysiological mechanisms and clinical manifestations of AAS-induced cardiomyopathy. Chronic supraphysiologic AAS use promotes cardiac injury and adverse cardiac remodeling via oxidative stress, androgen receptor overactivation, RAAS dysregulation, and pro-apoptotic signaling. These changes could lead to hypertension, dyslipidemia and atherosclerosis, myocardial fibrosis and hypertrophy, arrhythmias, heart failure, and kidney injury. Vascular dysfunction, increased arterial stiffness, and a prothrombotic state further compound the cardiovascular risks. Diagnostic approaches involve biomarker evaluation, echocardiography, and cardiac magnetic resonance imaging, revealing structural and functional cardiac abnormalities such as reduced ejection fraction, concentric hypertrophy, myocardial fibrosis, and impaired diastolic function. Although cessation of AAS use may lead to partial or complete reversal of cardiac dysfunction in some individuals, others may experience irreversible myocardial damage. The reversibility appears to depend on dosage, duration of exposure, and early intervention. This review explores the cardiovascular consequences of AAS use, with a focus on the mechanisms, diagnosis, and management of AAS-induced cardiomyopathy, and underlines the importance of education and early detection.