Incidence and prognosis of apparent-treatment resistant hypertension: a multi-state analysis using real world evidence.

Relation of Baseline Systolic Blood Pressure and Long-Term Outcomes in Ambulatory Patients With Chronic Mild to Moderate Heart Failure

Rapid fluid removal during dialysis is associated with cardiovascular morbidity and mortality

Ambulatory Blood Pressure in Chronic Kidney Disease: Ready for Prime Time?

J-curve for DBP and cardiovascular mortality in coronary artery disease patients

World Kidney Day 2011: Protect Your Kidneys, Save Your Heart

COVID-19, hypertension, and renin-angiotensin-aldosterone system inhibitors: Much ado about nothing or real problem to be solved?

### CONTRIBUTION OF THE AREA POSTREMA TO THE INCREASED CARDIAC SYMPATHETIC NERVE ACTIVITY IN OVINE HEART FAILURE Abukar Y, Ramchandra R, May CN The Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia Background : Heart failure (HF) is associated with an increase in cardiac sympathetic nerve activity (CSNA), which is directly linked to mortality in HF patients. The mechanisms responsible for the elevated CSNA remain unclear. Previous studies indicate that the area postrema (AP), a circumventricular organ in the brainstem, plays a role in the control of sympathetic nerve activity. We hypothesized that the elevated CSNA in HF is mediated by the AP and lesioning this region would reduce the increased CSNA in sheep with HF. Aims : To determine the effect of sham lesion or lesion of the AP on CSNA and hemodynamics in conscious sheep with HF. Methods : Studies were conducted in 2 groups of sheep with pacing-induced HF: sham (n=6) and AP lesion (n=6) sheep. Mean arterial blood pressure (MAP), heart rate (HR) and CSNA were recorded simultaneously in conscious sheep at least 4 days after surgery. Results : Heart failure was associated with a significant decrease in ejection fraction (from 74±2 % to 38±1 %; P<0.001), which was similar in both groups. There was a significant reduction in CSNA burst incidence in the AP lesion group compared with the sham group (45±10 and 89±3 bursts/100 heartbeats, respectively; P<0.01). Conclusions : In sheep with HF, the group with lesion of the AP had a significantly lower CSNA compared with the sham group. These data suggest that the AP plays a role in setting the detrimental high levels of CSNA in HF. ### G PROTEIN-COUPLED ESTROGEN RECEPTOR SIGNALING IMPROVES STROKE OUTCOME IN FEMALE MICE Broughton BRS, Jansen GL, Sobey CG Department of Pharmacology, Monash University, Clayton, Victoria, Australia Background: Estrogen has been assumed to provide neuroprotection following stroke entirely via classical estrogen receptors. Interestingly, there is recent evidence that activation of a novel G …

1. Relationship Between Hypertension and CAD e437 2. Prevention of Cardiovascular Events in Patients With Hypertension and CAD e443 3. BP Goals e445 4. Management of Hypertension in Patients With CAD and Stable Angina e449 5. Management of Hypertension in Patients With ACS e451

Background Vascular endothelial growth factor D (VEGF-D) is a secreted glycoprotein that can induce lymphangiogenesis and angiogenesis. We recently demonstrated that serum levels of VEGF-D are independently associated with all-cause mortality in patients with suspected or known coronary artery disease (CAD). However, the impact of chronic kidney disease (CKD) on the associations of VEGF-D with cardiovascular (CV) events and mortality in those patients is unclear. Methods Serum VEGF-D levels were measured in 2,418 patients with suspected or known CAD undergoing elective coronary angiography. The primary outcome was CV death. The secondary outcomes were all-cause death, major adverse CV events (MACE) defined as a composite of CV death, nonfatal myocardial infarction, and nonfatal stroke, and heart failure (HF) hospitalization. Patients were divided into 2 groups according to the presence (CKD, n=999) or absence (non-CKD, n=1,419) of CKD, and followed up over a 6-year period. Results During the follow-up, 325 CKD and 211 non-CKD patients died from any cause, 116 CKD and 49 non-CKD patients died from CV disease, 173 CKD and 124 non-CKD patients developed MACE, and 169 CKD and 99 non-CKD patients developed HF hospitalization. After adjustment for potential clinical confounders and established CV biomarkers (i.e., N-terminal pro-brain natriuretic peptide, high-sensitivity cardiac troponin I, and high-sensitivity C-reactive protein), VEGF-D levels were significantly associated with CV death (hazard ratio [HR] for 1-SD increase, 1.20; 95% confidence interval [CI], 1.06–1.37), all-cause death (HR, 1.15; 95% CI, 1.05–1.25), MACE (HR, 1.15; 95% CI, 1.03–1.29), and HF hospitalization (HR, 1.15; 95% CI, 1.02–1.29) in CKD, while VEGF-D levels were significantly associated with HF hospitalization (HR, 1.27; 95% CI, 1.09–1.49), but not with CV death (HR, 0.98; 95% CI, 0.68–1.43), all-cause death (HR, 1.10; 95% CI, 0.94–1.28), or MACE (HR, 0.94; 95% CI, 0.74–1.20) in non-CKD patients. The addition of VEGF-D levels to the model with potential clinical confounders and established CV biomarkers significantly improved the prediction of CV death (P&amp;lt;0.001 for continuous net reclassification improvement [NRI], P= 0.046 for integrated discrimination improvement [IDI]) and all-cause death (P&amp;lt;0.001 for NRI, P=0.004 for IDI), but not that of MACE (P=0.001 for NRI, P= 0.080 for IDI) or HF hospitalization (P=0.542 for NRI, P=0.605 for IDI) in CKD, whereas the addition of VEGF-D levels did not improve the prediction of CV death (P=0.769 for NRI, P=0.717 for IDI), all-cause death (P=0.089 for NRI, P=0.485 for IDI), MACE (P=0.876 for NRI, P=0.313 for IDI) or HF hospitalization (P=0.532 for NRI, P=0.155 for IDI) in non-CKD patients. Conclusions The VEGF-D level independently predicted CV and all-cause mortality in CKD, but not in non-CKD patients with suspected or known CAD. The associations of VEGF-D with CV and all-cause mortality may depend on the presence of CKD.

The Impact of APOL1 on Chronic Kidney Disease and Hypertension.

That elevated heart rate (HR) is a risk factor for cardiovascular morbidity and mortality in healthy people as well as in patients with cardiac diseases is supported by numerous epidemiological association studies.1–4 Increased HR has been recognized as a negative prognostic factor independent of many other clinical parameters that can influence the HR, including physical activity scores, left ventricular function, or use of β-blockers. Thus, HR appears to satisfy all epidemiological criteria for being considered as a true risk factor, and its predictive value for cardiovascular disease appeared to be as strong as that of most important cardiovascular risk factors. This is particularly true for the results obtained in hypertensive patients. Elevated HR is a common feature among hypertensive individuals.1 Among the young hypertensive subjects participating in the HARVEST study, >15% had a baseline resting HR ≥85 bpm and 27% had a HR ≥80 bpm.5 According to the Tensiopulse study, which evaluated 38 145 patients cared for by 2000 general practitioners all across Italy, >30% of the hypertensive patients had a resting HR ≥80 bpm.6 In a large French population, untreated hypertensive subjects had approximately a 6-bpm faster HR than normotensive individuals.7 Elevated HR is frequently associated with high blood pressure (BP) and metabolic disturbances and increases the risk of new onset hypertension and diabetes.1 Many experimental data obtained both in animals and in human beings support the importance of HR as a true risk factor for atherosclerosis and cardiovascular disease, providing convincing evidence for this pathogenetic mechanism.1–3 The pathogenetic connection between HR and cardiovascular disease has been discussed in several reports1–3,8,9 and is beyond the scope of this review. ### High HR as a Precursor of Hypertension, Obesity, and Diabetes Numerous studies have demonstrated that tachycardia is frequently associated with hypertension in …

Highlights From the Circulation Family of Journals.

Cardiovascular risk stratification: how important is the hypertensive response to exercise?

Renin-Angiotensin-Aldosterone System Inhibitors and Outcome in Patients With SARS-CoV-2 Pneumonia: A Case Series Study.

BackgroundChronic kidney disease (CKD) is very common in patients who are at a high risk of developing incident heart failure with reduced ejection fraction (HFrEF). However, the harmful effect of CKD on incident HFrEF has not yet been examined among patients with coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI).MethodsPatients undergoing PCI with baseline left ventricular ejection fraction (LVEF) ≥ 40% were included from January 2007 to December 2018 (ClinicalTrials.gov NCT04407936). We defined incident HFrEF as a follow-up LVEF of <40% within 3–12 months after discharge. Multivariable logistical regression was performed to examine the association of CKD with incident HFrEF.ResultsOverall, of 2,356 patients (mean age 62.4 ± 10.7 years, 22.2% women), 435 (18.5%) had CKD, and 83 (3.5%) developed incident HFrEF following PCI. The rate of incident HFrEF in the CKD group was higher than that in the non-CKD group (6.9 vs. 2.8%; p < 0.001). Multivariate logistic regression analysis indicated that CKD was an independent risk factor of incident HFrEF [adjusted odds ratio (aOR) = 1.75; 95% CI, 1.03–2.92; p = 0.035] after adjustment for confounders including age, gender, diabetes, hypertension, atrial fibrillation, congestive heart failure (CHF), baseline LVEF, ACEI/ARB, and statins. Furthermore, patients with incident HFrEF have a higher ratio of all-cause mortality compared to those without HFrEF (26.5 vs. 8.1%; p < 0.001).ConclusionsOur results suggested that CKD was associated with increased risk of incident HFrEF, which was related to higher all-cause mortality in patients with CAD undergoing PCI. On this basis, more aggressive measures should be taken to prevent patients with CKD undergoing PCI from developing HFrEF.