The relative associations of aortic and carotid artery stiffness with CeVD and cognition.

We examined the relative associations of aortic and carotid artery stiffness with cerebrovascular disease (CeVD), cognition, and dementia subtypes in a memory clinic cohort of 272 participants (mean age = 75.4, SD = 6.8). We hypothesized that carotid artery stiffness would have greater effects on outcomes, given its proximate relationship to the brain. Aortic and carotid artery stiffness were assessed with applanation tonometry and carotid ultrasonography, respectively. CeVD markers included white matter hyperintensities (WMH), lacunes, cerebral microbleeds, cortical infarcts, and intracranial stenosis. Cognition was assessed by the Mini Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and a neuropsychological battery. Multivariable linear regression was conducted to determine associations of arterial stiffness with WMH and cognition, while logistic regression analysed associations with CeVD markers and dementia subtypes. Carotid artery stiffness z-score was associated with WMH, cortical infarcts, vascular cognitive impairment, and MMSE, independent of age, sex, education, vascular risk factors, and aortic stiffness z-score. Although aortic stiffness z-score was independently associated with cortical infarcts, this became non-significant after further adjusting for carotid artery stiffness z-score. We found that carotid artery stiffness had greater effects on CeVD, cognitive function and impairment in memory clinic patients compared to aortic stiffness.

Cornell product is an ECG marker of heart failure with preserved ejection fraction.

OBJECTIVE: ECG markers of heart failure (HF) with preserved ejection fraction (HFpEF) are lacking. We hypothesised that the Cornell product (CP) is a risk marker of HFpEF and has prognostic utility in HFpEF. METHODS: CP =[(amplitude of R wave in aVL+depth of S wave in V3)×QRS] was measured on baseline 12-lead ECG in a prospective Asian population-based study of 606 healthy controls (aged 55±10 years, 45% men), 221 hypertensive controls (62±9 years, 58% men) and 242 HFpEF (68±12 years, 49% men); all with EF ≥50% and followed for 2 years for all-cause mortality and HF hospitalisations. RESULTS: CP increased across groups from healthy controls to hypertensive controls to HFpEF, and distinguished between HFpEF and hypertension with an optimal cut-off of ≥1800 mm*ms (sensitivity 40%, specificity 85%). Age, male sex, systolic blood pressure (SBP) and heart rate were independent predictors of CP ≥1800 mm*ms, and CP was associated with echocardiographic E/e' (r=0.27, p<0.01) and left ventricular mass index (r=0.46, p<0.01). Adjusting for clinical and echocardiographic variables and log N-terminal pro B-type natriuretic peptide (NT-proBNP), CP ≥1800 mm*ms was significantly associated with HFpEF (adjusted OR 2.7, 95% CI 1.0 to 7.0). At 2-year follow-up, there were 29 deaths and 61 HF hospitalisations, all within the HFpEF group. Even after adjusting for log NT-proBNP, clinical and echocardiographic variables, CP ≥1800 mm*ms remained strongly associated with a higher composite endpoint of all-cause mortality and HF hospitalisations (adjusted HR 2.1, 95% CI 1.2 to 3.5). CONCLUSION: The Cornell product is an easily applicable ECG marker of HFpEF and predicts poor prognosis by reflecting the severity of diastolic dysfunction and LV hypertrophy.