Screening for hypertension in adults: protocol for evidence reviews to inform a Canadian Task Force on Preventive Health Care guideline update.

Purpose: To inform updated recommendations by the Canadian Task Force on Preventive Health Care on screening in a primary care setting for hypertension in adults aged 18 years and older. This protocol outlines the scope and methods for a series of systematic reviews and one overview of reviews.

Methods: To evaluate the benefits and harms of screening for hypertension, the Task Force will rely on the relevant key questions from the 2021 United States Preventive Services Task Force systematic review.

Whither digitalis? What we can still learn from cardiotonic steroids about heart failure and hypertension.

Cloning of the "Na pump" (Na,K-ATPase or NKA) and identification of a circulating ligand, endogenous ouabain (EO), a cardiotonic steroid (CTS), triggered seminal discoveries regarding EO and its NKA receptor in cardiovascular function and the pathophysiology of heart failure (HF) and hypertension. Cardiotonic digitalis preparations were a preferred treatment for HF for two centuries, but digoxin was only marginally effective in a large clinical trial (1997). This led to diminished digoxin use.

The effects of high-intensity interval training, Nordic walking and moderate-to-vigorous intensity continuous training on functional capacity, depression and quality of life in patients with coronary artery disease enrolled in cardiac rehabilitation: A randomized controlled trial (CRX study).

Background: Coronary artery disease (CAD) patients undergoing revascularization procedures often experience ongoing, diminished functional capacity, high rates of depression and markedly low quality of life (QoL). In CAD patients, studies have demonstrated that high-intensity interval training (HIIT) is superior to traditional moderate-to-vigorous intensity continuous training (MICT) for improving functional capacity, whereas no differences between Nordic walking (NW) and MICT have been observed. Mental health is equally as important as physical health, yet few studies have examined the impact of HIIT and NW on depression and QoL.

Effects of CPAP on Blood Pressure and Sympathetic Activity in Patients With Diabetes Mellitus, Chronic Kidney Disease, and Resistant Hypertension.

Background: Patients with obstructive sleep apnea (OSA) have increased sympathetic activity and frequently also have resistant hypertension (HTN). Treatment of OSA with continuous positive airway pressure (CPAP) decreases awake and sleep blood pressure (BP) and sympathetic activity. This study was designed to assess the effect of treatment of OSA with CPAP on sympathetic activity and BP in patients with diabetes mellitus (DM), chronic kidney disease (CKD), and resistant HTN.

Effects of exercise on BDNF-TrkB signaling in the paraventricular nucleus and rostral ventrolateral medulla in rats post myocardial infarction.

Brain-derived neurotrophic factor (BDNF)-tropomyosin-related kinase B (TrkB) signaling in the paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) is associated with cardiovascular regulation. Exercise increases plasma BDNF and attenuates activation of central pathways in the PVN and RVLM post myocardial infarction (MI). The present study assessed whether MI alters BDNF-TrkB signaling and intracellular factors Ca/calmodulin-dependent protein kinase II (CaMKII) and Akt in the PVN and RVLM of male Wistar rats with or without exercise or treatment with the TrkB blocker ANA-12.

Can heat therapy help patients with heart failure?

To review and analyze the clinical outcomes of thermal therapy (≤1.4°C increase in core body temperature) in patients with heart failure (HF). A systematic review and meta-analysis regarding the effects of thermal therapy on HF was done by searching PubMed, Ovid Medline, Ovid Embase, Scopus, and internal databases up to date (2019).

Sodium pumps, ouabain and aldosterone in the brain: A neuromodulatory pathway underlying salt-sensitive hypertension and heart failure.

Accumulating evidence obtained over the last three decades has revealed a neuroendocrine system in the brain that mediates long term increases in blood pressure. The system involves distinct ion transport pathways including the alpha-2 isoform of the Na,K pump and epithelial sodium channels, as well as critical hormone elements such as angiotensin II, aldosterone, mineralocorticoid receptors and endogenous ouabain. Activation of this system either by circulating or central sodium ions and/or angiotensin II leads to a cascading sequence of events that begins in the hypothalamus and involves the participation of several brain nuclei including the subfornical organ, supraoptic and paraventricular nuclei and the rostral ventral medulla.

Effect of exercise training on the FNDC5/BDNF pathway in spontaneously hypertensive rats.

Increased sympathetic activity contributes to the development of cardiovascular diseases such as hypertension. Exercise training lowers sympathetic activity and is beneficial for the prevention and treatment of hypertension and associated cognitive impairment. Increased BDNF expression in skeletal muscle, heart, and brain may contribute to these actions of exercise, but the mechanisms by which this occurs are unknown.

Role of Myocardial Infarction-Induced Neuroinflammation for Depression-Like Behavior and Heart Failure in Ovariectomized Female Rats.

After myocardial infarction (MI), ovariectomized (OVX) female rats develop depression-like behaviors and an increase of pro-inflammatory cytokine (PIC) levels in the prefrontal cortex (PFC). We hypothesized that inhibition of neuroinflammation by the PIC synthesis inhibitor, pentoxifylline (PTX) would prevent depression-like behaviors induced by heart failure (HF) post-MI in OVX female rats. PTX treatment was initiated in female Wistar rats, 1 week after ovariectomy, and 1 week before MI by occlusion of the left anterior descending artery.

Inhibition of inflammation by minocycline improves heart failure and depression-like behaviour in rats after myocardial infarction.

Rationale: Patients with heart failure have an increased incidence of depression. Central and peripheral inflammation play a major role in the pathophysiology of both heart failure and depression.

Aim: Minocycline is an antibiotic that inhibits microglia activation and release of pro-inflammatory cytokines.

Use of Directly Observed Therapy to Assess Treatment Adherence in Patients With Apparent Treatment-Resistant Hypertension.

This cohort study evaluates the association of directly observed therapy with treatment adherencee in patients with apparent treatment-resistant hypertension.

Specific Inhibition of Brain Angiotensin III Formation as a New Strategy for Prevention of Heart Failure After Myocardial Infarction.

Aims: Inhibition of brain angiotensin III by central infusion of aminopeptidase A (APA) inhibitor firibastat (RB150) inhibits sympathetic hyperactivity and heart failure in rats after myocardial infarction (MI). This study evaluated effectiveness of systemic treatment with firibastat compared with AT1R blocker, losartan.

Methods And Results: MI was induced by ligation of left coronary artery in male Wistar rats.

Effects of exercise training and TrkB blockade on cardiac function and BDNF-TrkB signaling postmyocardial infarction in rats.

Exercise training is beneficial for preserving cardiac function postmyocardial infarction (post-MI), but the underlying mechanisms are not well understood. We investigated one possible mechanism, brain-derived neurotrophic factor (BDNF)-tropomyosin-related kinase B (TrkB) signaling, with the TrkB blocker ANA-12 (0.5 mg·kg·day).

Sex differences in depression-like behavior and neuroinflammation in rats post-MI: role of estrogens.

Patients with heart failure (HF) have a high prevalence of depression associated with a worse prognosis, particularly in older women. The present study evaluated whether sex and estrogens affect depression-like behavior and associated neuroinflammation induced by myocardial infarction (MI) in rats. MI was induced by occlusion of the left anterior descending artery in young adult male and female Wistar rats or in ovariectomized (OVX) female rats without and with estrogen [17β-estradiol (E)] replacement.

Central and peripheral slow-pressor mechanisms contributing to Angiotensin II-salt hypertension in rats.

Aims: High salt intake markedly enhances hypertension induced by angiotensin II (Ang II). We explored central and peripheral slow-pressor mechanisms which may be activated by Ang II and salt.

Methods And Results: In protocol I, Wistar rats were infused subcutaneously with low-dose Ang II (150 ng/kg/min) and fed regular (0.

Update on angiotensin II: new endocrine connections between the brain, adrenal glands and the cardiovascular system.

In the brain, angiotensinergic pathways play a major role in chronic regulation of cardiovascular and electrolyte homeostasis. Increases in plasma angiotensin II (Ang II), aldosterone, [Na] and cytokines can directly activate these pathways. Chronically, these stimuli also activate a slow neuromodulatory pathway involving local aldosterone, mineralocorticoid receptors (MRs), epithelial sodium channels and endogenous ouabain (EO).

Cardiotrophin 1 stimulates beneficial myogenic and vascular remodeling of the heart.

The post-natal heart adapts to stress and overload through hypertrophic growth, a process that may be pathologic or beneficial (physiologic hypertrophy). Physiologic hypertrophy improves cardiac performance in both healthy and diseased individuals, yet the mechanisms that propagate this favorable adaptation remain poorly defined. We identify the cytokine cardiotrophin 1 (CT1) as a factor capable of recapitulating the key features of physiologic growth of the heart including transient and reversible hypertrophy of the myocardium, and stimulation of cardiomyocyte-derived angiogenic signals leading to increased vascularity.

Expertise: no longer a sine qua non for guideline authors?

: Several sets of guidelines have been published recently and more are in the works. The very recent American College of Physicians/American Academy of Family Practitioners guidelines were put together by a set of authors and consultants without any expertise in the topic under discussion, that is, hypertension. Although we are not maintaining that all guidelines should be written exclusively by experts, complete lack of expertise among guideline authors is not acceptable.

Effects of exercise training on brain-derived neurotrophic factor in skeletal muscle and heart of rats post myocardial infarction.

What is the central question of this study? Exercise training increases brain-derived neurotrophic factor (BDNF) in the hippocampus, which depends on a myokine, fibronectin type III domain-containing protein 5 (FNDC5). Whether exercise training after myocardial infarction induces parallel increases in FNDC5 and BDNF expression in skeletal muscle and the heart has not yet been studied. What is the main finding and its importance? Exercise training after myocardial infarction increases BDNF protein in skeletal muscle and the non-infarct area of the LV without changes in FNDC5 protein, suggesting that BDNF is not regulated by FNDC5 in skeletal muscle and heart.

On-treatment blood pressures of older hypertensive patients in Canada: implications for Systolic blood PRessure INtervention Trial.

Objective: The therapeutic target level for the blood pressure (BP) on antihypertensive drug treatment in older hypertensive patients is still extensively debated. We assessed the achieved BP levels in older treated hypertensive patients in a representative sample of the population.

Design: During the 2006 Ontario Survey on the Prevalence and Control of Hypertension, BP (using the SPRINT protocol) and treatment data were collected in 2551 respondents from a random and representative sample of the adult (20-79 years) population.

Pivotal role of α2 Na pumps and their high affinity ouabain binding site in cardiovascular health and disease.

Reduced smooth muscle (SM)-specific α2 Na pump expression elevates basal blood pressure (BP) and increases BP sensitivity to angiotensin II (Ang II) and dietary NaCl, whilst SM-α2 overexpression lowers basal BP and decreases Ang II/salt sensitivity. Prolonged ouabain infusion induces hypertension in rodents, and ouabain-resistant mutation of the α2 ouabain binding site (α2 mice) confers resistance to several forms of hypertension. Pressure overload-induced heart hypertrophy and failure are attenuated in cardio-specific α2 knockout, cardio-specific α2 overexpression and α2 mice.