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In their recent guidelines, the European Society of Hypertension upgraded β blockers, putting them on equal footing with thiazide diuretics, renin-angiotensin system blockers (eg, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers), and calcium channel blockers. The reason offered for upgrading β blockers was the observation that they are often used for many other clinical conditions commonly encountered with hypertension. This upgrade would allow for the treatment of two conditions with a single drug (a so-called twofer). In most current national and international hypertension guidelines, β blockers are only considered to be an alternative when there are specific indications. Compared with the other first-line antihypertensive drug classes, β blockers are significantly less effective in preventing stroke and cardiovascular mortality. To relegate β blockers to an inferiority status as previous guidelines have done was based on the evidence in aggregate, and still stands. No new evidence supports the switch of β blockers back to first-line therapy. We are concerned that this move might lead to widespread harm because of inferior stroke protection., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background and Purpose: Assisted reproductive technologies (ART) induce premature vascular aging in human offspring. The related alterations are well-established risk factors for stroke and predictors of adverse stroke outcome. However, given the young age of the human ART population there is no information on the incidence and outcome of cerebrovascular complications in humans. In mice, ART alters the cardiovascular phenotype similarly to humans, thereby offering the possibility to study this problem., Methods: We investigated the morphological and clinical outcome after ischemia/reperfusion brain injury induced by transient (45 min) middle cerebral artery occlusion in ART and control mice., Results: We found that stroke volumes were almost 3-fold larger in ART than in control mice (P < 0.001). In line with these morphological differences, neurological performance assessed by the Bederson and RotaRod tests 24 and 48 h after artery occlusion was significantly worse in ART compared with control mice. Plasma levels of TNF-alpha, were also significantly increased in ART vs. control mice after stroke (P < 0.05). As potential underlying mechanisms, we identified increased blood-brain barrier permeability evidenced by increased IgG extravasation associated with decreased tight junctional protein claudin-5 and occludin expression, increased oxidative stress and decreased NO-bioactivity in ART compared with control mice., Conclusions: In wildtype mice, ART predisposes to significantly worse morphological and functional stroke outcomes, related at least in part to altered blood-brain barrier permeability. These findings demonstrate that ART, by inducing premature vascular aging, not only is a likely risk factor for stroke-occurrence, but also a mediator of adverse stroke-outcome., Translational Perspective: This study highlights that ART not only is a likely risk factor for stroke-occurrence, but also a mediator of adverse stroke-outcome. The findings should raise awareness in the ever-growing human ART population in whom these techniques cause similar alterations of the cardiovascular phenotype and encourage early preventive and diagnostic efforts., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Longstanding hypertension ultimately leads to heart failure (HF), and, as a consequence most patients with HF have a history of hypertension. Conversely, absence of hypertension in middle age is associated with lower risks for incident HF across the remaining life course. Cardiac remodeling to a predominant pressure overload consists of diastolic dysfunction and concentric left ventricular (LV) hypertrophy. When pressure overload is sustained, diastolic dysfunction progresses, filling of the concentric remodeled LV decreases, and HF with preserved ejection fraction ensues. Diastolic dysfunction and HF with preserved ejection fraction are the most common cardiac complications of hypertension. The end stage of hypertensive heart disease results from pressure and volume overload and consists of dilated cardiomyopathy with both diastolic dysfunction and reduced ejection fraction. "Decapitated hypertension" is a term used to describe the decrease in blood pressure resulting from reduced pump function in HF. Progressive renal failure, another complication of longstanding hypertension, gives rise to the cardiorenal syndrome (HF and renal failure). The so-called Pickering syndrome, a clinical entity consisting of flash pulmonary edema and bilateral atheromatous renovascular disease, is a special form of the cardiorenal syndrome. Revascularization of renal arteries is the treatment of choice. Most antihypertensive drug classes when used as initial therapy decelerate the transition from hypertension to HF, although not all of them are equally efficacious. Low-dose, once-daily hydrochlorothiazide should be avoided, but long-acting thiazide-like diuretics chlorthalidone and indapamide seem to have an edge over other antihypertensive drugs in preventing HF., (Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: Takotsubo Cardiomyopathy (TTC) is commonly triggered by acute illness, physical or emotional stress and has been associated with elevated catecholamine levels. TTC has also been associated with pheochromocytoma (TTC-pheo)., Methods: We performed a computer assisted search of the electronic databases Medline, Scopus and Google Scholar from 1965 to January 2011. All case reports with reported TTC-pheo were selected and compared to a recent review by Gianni et al. which examined primary TTC (TTC-primary)., Statistics: Data analysis was performed using SPSS version 18. Chi-square test of Fisher's exact test was used as appropriate to compare categorical data., Results: 38 cases of TTC-pheo were retrieved from literature and compared to 254 cases of TTC-p. Chest pain was the most common presentation in both groups. The TTC-pheo patients were on average 18 years younger than patients with TTC-p (p<0.01). Only a minority of TTC-pheo patients presented with classical features of pheochromocytoma including hypertension (52.6%), headache (28.9%), palpitations (31.6 %), and diaphoresis (26.3%). In TTC-pheo complications rates were higher compared to TTC-p, including cardiogenic shock (34.2% vs. 4.2%, p<0.01) and heart failure (46.7% vs. 17.7%, p<0.01). Antecedent stressors were less common in TTC-pheo. About one-third of TTC-pheo patients presented with the inverted pattern, which compared to the apical pattern, was associated with higher complication rates, including, cardiogenic shock, heart failure, acute renal failure and arrhythmias., Conclusions: Although rare, pheochromocytoma should be considered in the differential diagnosis of TTC especially in younger patients presenting without antecedent stressors and a high complication rate. The similarities in the clinical features and outcomes in patients with TTC-p and TTC-pheo point to a similar underlying cardiac pathophysiologic process at the time of the acute presentation., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Increase in pulse pressure has been shown to be predisposing factor for Coronary Artery Disease (CAD) in diverse patient populations but its relationship with the severity of CAD, particularly in the South Asians immigrant population of United States has not been demonstrated. We performed a single-center, cross-sectional study. Pulse pressure was calculated by the difference between the systolic and diastolic brachial blood pressures, and the Friesinger score (FS) was used to quantify the severity of CAD with the score of 5 used as a cutoff for extensive disease. We also sought to assess the correlation between the Friesinger score and the 10-year cardiovascular event (CVD) risk as calculated by the Framingham score. Odds ratios and 95% confidence intervals for the associations between explanatory variables and a high Friesinger score were estimated using multivariate logistic regression models. P values below .05 were considered to be statistically significant. Statistical analysis was performed using STATA version 10 software package (College Station, TX). The mean pulse pressure was significantly higher in participants with an FS of > or =5 compared with participants with an FS of <5 (63 vs. 46 mm Hg; P = .004). In univariate analysis, a pulse pressure > or =40 mm Hg was associated with a five-fold increased odds of a higher FS compared with a pulse pressure <40 mm Hg (P = .039), which was unchanged in multivariate analysis. In multivariate analysis, even after adjustment for presence of hypertension, a 10 mm Hg increase in pulse pressure was associated with a 1.97-fold increased odds of a higher FS (95% CI 1.22-3.71, P = .009). The mean Framingham score was higher in participants with a higher FS, but this difference was not significant (32.7 vs. 20.3; P = .1139). Our study demonstrates that pulse pressure, a well-established marker of vascular health, is a significant independent predictor of the severity of CAD as assessed by coronary angiography in South Asians., (Copyright (c) 2010 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Background: American College of Cardiology and American Heart Association (ACC/AHA) guidelines on perioperative assessment recommend perioperative beta blockers for non-cardiac surgery, although results of some clinical trials seem not to support this recommendation. We aimed to critically review the evidence to assess the use of perioperative beta blockers in patients having non-cardiac surgery., Methods: We searched Pubmed and Embase for randomised controlled trials investigating the use of beta blockers in non-cardiac surgery. We extracted data for 30-day all-cause mortality, cardiovascular mortality, non-fatal myocardial infarction, non-fatal stroke, heart failure, and myocardial ischaemia, safety outcomes of perioperative bradycardia, hypotension, and bronchospasm., Findings: 33 trials included 12 306 patients. beta blockers were not associated with any significant reduction in the risk of all-cause mortality, cardiovascular mortality, or heart failure, but were associated with a decrease (odds ratio [OR] 0.65, 95% CI 0.54-0.79) in non-fatal myocardial infarction (number needed to treat [NNT] 63) and decrease (OR 0.36, 0.26-0.50) in myocardial ischaemia (NNT 16) at the expense of an increase (OR 2.01, 1.27-3.68) in non-fatal strokes (number needed to harm [NNH] 293). The beneficial effects were driven mainly by trials with high risk of bias. For the safety outcomes, beta blockers were associated with a high risk of perioperative bradycardia requiring treatment (NNH 22), and perioperative hypotension requiring treatment (NNH 17). We recorded no increased risk of bronchospasm., Interpretation: Evidence does not support the use of beta-blocker therapy for the prevention of perioperative clinical outcomes in patients having non-cardiac surgery. The ACC/AHA guidelines committee should soften their advocacy for this intervention until conclusive evidence is available.

Essential hypertension can be defined as a rise in blood pressure of unknown cause that increases risk for cerebral, cardiac, and renal events. In industrialised countries, the risk of becoming hypertensive (blood pressure >140/90 mm Hg) during a lifetime exceeds 90%. Essential hypertension usually clusters with other cardiovascular risk factors such as ageing, being overweight, insulin resistance, diabetes, and hyperlipidaemia. Subtle target-organ damage such as left-ventricular hypertrophy, microalbuminuria, and cognitive dysfunction takes place early in the course of hypertensive cardiovascular disease, although catastrophic events such as stroke, heart attack, renal failure, and dementia usually happen after long periods of uncontrolled hypertension only. All antihypertensive drugs lower blood pressure (by definition) and this decline is the best determinant of cardiovascular risk reduction. However, differences between drugs exist with respect to reduction of target-organ disease and prevention of major cardiovascular events. Most hypertensive patients need two or more drugs for blood-pressure control and concomitant statin treatment for risk factor reduction. Despite the availability of effective and safe antihypertensive drugs, hypertension and its concomitant risk factors remain uncontrolled in most patients.

With the aging of the population, the incidence and prevalence of cognitive disorders are increasing. Blood pressure plays an important role in the pathogenesis or clinical progression of stroke, vascular dementia, and Alzheimer's disease. Data from different studies reveal that the uses of antihypertensive medications decrease the risk of dementia and cognitive dysfunction. Several studies also have demonstrated a relationship between hypotension, cognitive decline, and dementia. In this review we are trying to demonstrate the relationship between blood pressure and cognitive function and also the effect of antihypertensive medications on dementia and cognitive dysfunction.

Background: The clinical use of cyclosporine as an immunosuppressive agent enhanced long-term survival in transplant recipients at the expense of a high incidence of induced hypertension. Altered neurovegetative (autonomic) cardiovascular control is suspected as a mechanism of this form of hypertension., Methods: Spectral analysis of systolic arterial pressure and R-R interval variability (electrocardiographic recordings) were performed, and the index alpha of baroreflex gain was computed in four groups of subjects matched for age: 13 orthotopic heart transplant recipients; 13 solid organ transplant recipients; 13 patients with essential hypertension; and 18 control subjects with normal blood pressure. All but the control subjects were treated with similar dihydropyridine calcium entry blockers. Heart and solid organ transplant recipients also received cyclosporine., Results: R-R variance was lowest in the heart transplant recipients. The spectral profile of R-R interval was suggestive of sympathetic predominance in the patients with hypertension, but not in the solid organ transplant recipients or the control subjects. Systolic blood pressure variability and low frequency component (a marker of sympathetic vasomotor modulation) were similar in the four groups. The index alpha was 1.8 +/- 2.2 in heart transplant recipients, 11.7 +/- 6.6 in solid organ transplant recipients, 7.3 +/- 3.6 in patients with hypertension, and 13.5 +/- 6.4 msec/mm Hg in control subjects (p = 0.0001)., Conclusions: These data indicate that (1) cyclosporine-induced hypertension in heart transplant recipients is associated with a loss of baroreflex function as a result of cardiac denervation-related uncoupling; (2) compared with patients with hypertension, organ transplant recipients with hypertension demonstrated a maintained baroreflex function as indicated by a lack of reduction of the index alpha; (3) baroreflex heart rate control in dihydropyridine-treated cyclosporine-induced hypertension is well maintained.

Left-ventricular hypertrophy (LVH), the primary cardiac manifestation of hypertension, has been identified as the most powerful risk factor for future cardiovascular events causing morbidity and mortality, such as myocardial infarction, congestive heart failure, sudden death, and so forth. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left-ventricular filling and contractility. Besides hypertension, other risk factors such as obesity, advanced age, valvular heart disease, and other pathologic disorders can cause an increase in the hemodynamic burden and lead to LVH. Nonhemodynamic determinants of left-ventricular mass include dietary salt intake, alcohol, and neurohormones. LVH and its sequelae can be reduced by specific antihypertensive therapy, but despite these promising findings, future epidemiologic studies are necessary to document the clinical benefits of a reduction in LVH.

Red blood cell mass, plasma volume, and renal and systemic hemodynamic measurements were evaluated in 24 normotensive men (group 1), 45 men with mild essential hypertension (group 2), and 43 men with moderate to severe essential hypertension (group 3). Despite significant hemodynamic differences between the groups and although plasma volume was contracted, the increased hematocrit in the third group of patients was not explained by an increase in red blood cell mass. Because this was the case in all groups, it demonstrates that the increased hematocrit in patients with more severe essential hypertension is solely attributable to the contracted plasma volume.

A number of therapeutic agents, foods, chemicals, and poisons have been associated with the development or exacerbation of hypertension. This review discusses those identified in recent years.

Although often coexisting in the same patient, obesity and essential hypertension exert disparate cardiovascular effects. An excess of adipose tissue augments cardiac output, stroke volume, and left ventricular filling pressure, expands intravascular volume, and lowers total peripheral resistance. In contrast, essential hypertension in a non-obese patient is associated with a contracted intravascular volume, high total peripheral resistance, and normal cardiac output, but increased left ventricular stroke work due to high afterload. Left ventricular adaptation will consist of eccentric hypertrophy in the obese (irrespective of arterial pressure) and concentric hypertrophy in the non-obese hypertension patient. The combination of obesity and hypertension burdens the heart with high preload and high afterload, thereby greatly enhancing the risk of congestive heart failure. Peripheral resistance and intravascular volume may be normal in mildly hypertension obese patients because of the mutually antagonising effects of the increase in arterial pressure and the increase in body weight. The fall in arterial pressure associated with weight loss seems to be caused by a decrease in adrenergic activity which leads to a fall in cardiac output without change in vascular resistance. Obesity hypertension may be the result of an inappropriately raised cardiac output in the presence of a relatively restricted arterial capacity due to the low vascularity of adipose tissue. In morbid obesity increased blood viscosity may contribute to the raised arterial pressure.

To assess patterns of left ventricular adaptation, 38 patients with borderline and 38 with sustained mild essential hypertension, all lacking electrocardiographic and roentgenographic criteria for left ventricular hypertrophy, were compared using systemic hemodynamic values and M-mode echocardiograms. All patients had normal left ventricular function and measurements of wall thickness. Those with borderline hypertension showed no asymmetric increase in the ratio of septal to posterior wall thickness. The ratio of the left ventricular radius to wall thickness remained normal in both groups, indicating no disproportionate hypertrophy or dilatation of chambers during the phase of normal left ventricular function. Neither finding substantiates asymmetric septal hypertrophy in early hypertension. Those with mild essential hypertension demonstrated an augmented mean circumferential fiber shortening rate compared to those with borderline hypertension (P less than 0.005), suggesting an early stage of left ventricular hyperfunction in the development and elaboration of hypertensive heart disease.

In so-called essential hypertension, at least three different subsets of pathophysiologic findings can be identified: mild hypertension in nonobese juvenile subjects characterized by elevated cardiac output, normal peripheral resistance, increased sympathetic activity as measured by norepinephrine and plasma renin activity; hypertension in the elderly with a low cardiac output, often with left ventricular hypertrophy, elevated total peripheral resistance, nephrosclerosis contracted intravascular volume, and low plasma renin activity; and obese hypertensive patients with a high cardiac output, expanded intravascular volume, and a normal total peripheral resistance. Although there is often an overlap among these three entities, antihypertensive treatment can easily be adapted accordingly. A beta-adrenoreceptor blocker is the step-one drug to be used in mild hypertension with an elevated cardiac output. The drug's negative inotropic and chronotropic properties will bring the elevated cardiac output and heart rate back to normal. In the elderly hypertensive patient, an arteriolar and venous vasodilator, such as an antiadrenergic agent, slow channel calcium blocker, or a converting enzyme inhibitor, will lower total peripheral resistance and unburden the left ventricle. In the obese patient and also in most black subjects, the first-step antihypertensive agent remains a thiazide diuretic. Labetalol, an agent with both beta- and alpha-adrenoreceptor properties, shows promise for the treatment of hypertension in the young as well as in the older patient. It seems to be the agent of choice in patients with established essential hypertension who are concomitantly suffering from coronary artery disease.

In this article, the most important risk factors that may predict the transition from borderline to established hypertension are reviewed. Primary prevention has to focus on identifying individuals who are at highest risk and delaying or reversing further elevation of arterial pressure levels. A review of the literature indicates that several environmental and congenital factors can be identified as risk factors for the development of hypertension, including family history of essential hypertension, age, race, obesity, alcohol consumption, salt intake, hormonal status, and some stress factors. Of all diagnostic approaches to predict the development of hypertension, measurements of resting heart rate and responses to dynamic exercise have some predictive value.

Electrocardiograms and M-mode echocardiograms were evaluated in lean and obese patients, either normotensive or hypertensive, who were paired for mean arterial pressure, age, and sex. Electrocardiographic evidence of left atrial abnormalities (LAA) occurred more frequently (p less than 0.01) and left atrial size was greater in the obese than in the lean patients (p less than 0.01). The left atrial emptying index, an indicator of early diastolic ventricular function, was reduced in obese patients (p less than 0.01), most markedly in those with obesity-hypertension. The left atrial emptying index was reduced in obese patients with electrocardiographic LAA compared to obese patients without this electrocardiographic sign (p less than 0.02). A close correlation (r = 0.61, p less than 0.001) was obtained between the left atrial emptying index and atrial ECG abnormalities. These left atrial abnormalities in obesity and particularly in obesity-hypertension indicate diastolic ventricular dysfunction.

Whether or not obesity per se is an independent risk factor remains controversial. However, a variety of studies have shown that obesity precipitates certain well-known risk factors, such as glucose intolerance, hyperlipidemia, hyperestrogenemia, hypertension, and left ventricular hypertrophy. Distribution of adipose tissue also seems to influence cardiovascular risk; patients with predominantly male-pattern obesity exhibit more profound risk for cardiovascular disease.

Combined systolic and diastolic arterial hypertension and isolated systolic hypertension in the elderly are proven risk factors for stroke, sudden death, coronary artery disease, and congestive heart failure. Because hemodynamics, vascular and cardiac adaptations, fluid volume, and endocrine functions are distinctly altered in the elderly hypertensive patient compared with a younger patient, antihypertensive treatment should be individualized, and an unsophisticated regimen, such as a stepped-care approach, is too rigid to be as beneficial for elderly hypertensive patients as for young hypertensive patients.

In an attempt to dissociate the cardiovascular adaptations to high blood pressure from those of ageing, 30 patients with established essential hypertension aged over 65 years were matched for mean arterial pressure, race, sex, height, and weight with 30 patients younger than 42 years. Cardiac output, heart rate, stroke volume, intravascular volume, renal blood flow, and plasma renin activity were significantly lower in the elderly, whereas total peripheral (and renal vascular) resistance, left ventricular posterior wall and septal thicknesses, and left ventricular mass were higher. Intravascular volume correlated inversely with total peripheral resistance in both groups and in all patients. Pathophysiological findings of essential hypertension in the elderly are characterised by a hypertrophied heart of the concentric type with a low cardiac output resulting from a smaller stroke volume and a slower heart rate. Renal blood flow is disproportionally reduced and total peripheral and renal vascular resistance elevated.

Hypertension and obesity are two disorders that are closely related; each occurs more frequently with the other than in an otherwise normal population. These two disorders, however, exert disparate effects on cardiovascular structure and function. The hallmark of essential hypertension is an increased total peripheral resistance, and hypertensive patients have a contracted intravascular volume and normal cardiac output but an increased left ventricular stroke work due to a high afterload. In contrast, obese patients have an increased intravascular volume, left ventricular filling pressure, cardiac output and a lower total peripheral and renal vascular resistance. Left ventricular adaptation will consist of eccentric hypertrophy in obesity regardless of the level of arterial pressure and concentric hypertrophy in lean hypertensive patients. Although obesity may mitigate the harmful effect of a chronically elevated total peripheral and renal vascular resistance and lessen target organ damage in essential hypertension, the combination of obesity and hypertension presents a double burden to the left ventricle and is associated with systolic and diastolic dysfunction and a propensity for high grade ventricular dysrhythmias. It is not surprising that congestive heart failure and sudden death are common sequelae of obesity hypertension. Weight reduction reduces arterial pressure by decreasing intravascular volume and cardiac output associated with a fall in sympathetic activity and reversal of cardiac hypertrophy. Therefore, weight loss unloads the heart from the two-fold burden caused by obesity and hypertension and should become a major goal in the prevention and treatment of heart disease.

The pathophysiology and course of hypertensive cardiovascular disease in the black population differ significantly from those of nonblacks. The hemodynamic and endocrine profiles are different, consequences of hypertension are more severe in blacks, and black patients are often less responsive to standard antihypertensive treatment. Safe and efficacious treatment can be achieved when drug therapy is directed at the specific underlying pathophysiologic abnormality in black patients. By closely matching cardiovascular pathophysiologic findings in a given patient with the pharmacologic effects of an antihypertensive agent, blood pressure can often be controlled with fewer adverse effects. In addition, blood flow to target organs and their function can be maintained or improved. Calcium channel blockers are especially well suited for the treatment of essential hypertension in black patients.