Subclinical atherosclerosis underlies most cardiovascular diseases, manifesting before clinical symptoms and representing a key focus for early prevention strategies. Recent advancements highlight the importance of early detection and management of subclinical atherosclerosis. This review underscores that traditional risk factor levels considered safe, such as low-density lipoprotein cholesterol (LDL-C) and glycated haemoglobin (HbA1c), may still permit the development of atherosclerosis, suggesting a need for stricter thresholds. Early-life interventions are crucial, leveraging the brain's neuroplasticity to establish lifelong healthy habits. Preventive strategies should include more aggressive management of LDL-C and HbA1c from youth and persist into old age, supported by public health policies that promote healthy environments. Emphasising early education on cardiovascular health can fundamentally shift the trajectory of cardiovascular disease prevention and optimise long-term health outcomes.
Humans ; Atherosclerosis/diagnosis* ; Risk Factors ; Cardiovascular Diseases/prevention & control* ; Cholesterol, LDL/blood* ; Glycated Hemoglobin ; Cardiology/trends* ; Heart Disease Risk Factors

The heart-brain axis involves complex interactions between the cardiovascular and nervous systems via a network of cortical and subcortical structures working with the autonomic nervous system and intracardiac nervous system. Heart-brain interactions may be divided into 2 broad categories: cardiac effects of neurological disease and neurological effects of cardiac disease. The pathogenesis of neurogenic cardiac effects is thought to involve a neurogenic cascade where sudden shifts in autonomic balance lead to an exaggerated catecholamine release. This can occur in acute neurological conditions such as ischemic stroke, intracranial hemorrhage, and epilepsy. Cardiovascular complications include the stroke-heart syndrome, neurogenic pulmonary edema and cardiomyopathy, Takotsubo syndrome, arrhythmias, and even sudden cardiac death. Certain areas of the brain, such as the insular cortex, play key roles in cardiac autonomic regulation, and disorders affecting these areas have greater effects on the heart. On the other hand, cardiac conditions can also adversely impact the neurological system. Atrial fibrillation and left ventricular thrombus can cause cardioembolic strokes, whereas heart failure and severe aortic stenosis have been linked to the development of cognitive impairment. This review aims to provide a broad overview of key topics in neurocardiology as well as delve into the evidence and pathophysiology behind these conditions.

INTRODUCTION: Degenerative mitral stenosis (DMS) is frequently cited as increasing in prevalence in the developed world, although comparatively little is known about DMS in comparison to rheumatic mitral stenosis (RMS). METHOD: A retrospective observational study was conducted on 745 cases of native-valve mitral stenosis (MS) with median follow-up time of 7.25 years. Clinical and echocardiographic parameters were compared. Univariate and multivariate Cox regression analyses were performed for a composite of all-cause mortality and heart failure hospitalisation. RESULTS: Patients with DMS compared to RMS were older (age, mean ± standard deviation: 69.6 ± 12.3 versus [vs] 51.6 ± 14.3 years, respectively; P<0.001) and a greater proportion had medical comorbidities such as diabetes mellitus (78 [41.9%] vs 112 [20.0%], P<0.001). The proportion of cases of degenerative aetiology increased from 1.1% in 1991-1995 to 41.0% in 2016-2017. In multivariate analysis for the composite outcome, age (hazard ratio [HR] 95% confidence interval [CI] of 1.032 [1.020-1.044]; P<0.001), diabetes mellitus (HR 1.443, 95% CI 1.068-1.948; P=0.017), chronic kidney disease (HR 2.043, 95% CI 1.470-2.841; P<0.001) and pulmonary artery systolic pressure (HR 1.019, 95% CI 1.010- 1.027; P<0.001) demonstrated significant indepen-dent associations. The aetiology of MS was not independently associated with the composite outcome. CONCLUSION DMS is becoming an increasingly common cause of native-valve MS. Despite numerous clinical differences between RMS and DMS, the aetiology of MS did not independently influence a composite of mortality or heart failure hospitalisation.
Humans ; Mitral Valve Stenosis/etiology* ; Male ; Female ; Retrospective Studies ; Middle Aged ; Aged ; Rheumatic Heart Disease/mortality* ; Echocardiography ; Hospitalization/statistics & numerical data* ; Heart Failure/epidemiology* ; Singapore/epidemiology* ; Proportional Hazards Models ; Diabetes Mellitus/epidemiology*

The heart-brain axis involves complex interactions between the cardiovascular and nervous systems via a network of cortical and subcortical structures working with the autonomic nervous system and intracardiac nervous system. Heart-brain interactions may be divided into 2 broad categories: cardiac effects of neurological disease and neurological effects of cardiac disease. The pathogenesis of neurogenic cardiac effects is thought to involve a neurogenic cascade where sudden shifts in autonomic balance lead to an exaggerated catecholamine release. This can occur in acute neurological conditions such as ischemic stroke, intracranial hemorrhage, and epilepsy. Cardiovascular complications include the stroke-heart syndrome, neurogenic pulmonary edema and cardiomyopathy, Takotsubo syndrome, arrhythmias, and even sudden cardiac death. Certain areas of the brain, such as the insular cortex, play key roles in cardiac autonomic regulation, and disorders affecting these areas have greater effects on the heart. On the other hand, cardiac conditions can also adversely impact the neurological system. Atrial fibrillation and left ventricular thrombus can cause cardioembolic strokes, whereas heart failure and severe aortic stenosis have been linked to the development of cognitive impairment. This review aims to provide a broad overview of key topics in neurocardiology as well as delve into the evidence and pathophysiology behind these conditions.