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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial fibrillation is now the most common cardiac arrhythmia for which a patient is hospitalized. Clinically, it presents in a form that is paroxysmal, persistent, or permanent and may be symptomatic or asymptomatic, occurring in the setting of either no cardiac disease ("lone atrial fibrillation") or, most often, in association with an underlying disease. Atrial fibrillation is associated with a 2-fold increase in mortality and, in the United States alone, causes over 75,000 cases of stroke per year. The annual prevalence of stroke is 5% to 7%, but the use of adequate anticoagulation can reduce this to less than 1%. Atrial fibrillation is a disorder of the elderly, with almost equal prevalence in men and women. In the United States, 80% of atrial fibrillation occurs in patients over the age of 65 years, and its prevalence tracks that of heart failure, which may be the cause, as well as the result, of the arrhythmia. Both conditions are increasing in epidemic proportions in the aging population. The most common causes of atrial fibrillation are hypertensive heart disease, coronary artery disease, and heart failure with a miscellany of lesser conditions, with about 10% lacking structural heart disease. Unlike other supraventricular arrhythmias, cure by the use of catheter ablation and surgical techniques has not been a reality except in a relatively small number of cases. However, restoration and maintenance of sinus rhythm remain the initial goal of therapy for most patients. Pharmacologic approaches remain the mainstay of therapy for rate control and anticoagulation as well as for maintenance of sinus rhythm following pharmacological or electrical conversion. The changing epidemiology of atrial fibrillation is highlighted, with the focus on its conversion by the use of newer and novel antifibrillatory agents relative to the mechanisms of the arrhythmia, to restore the stability of sinus rhythm.
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PMID:Atrial fibrillation: epidemiologic considerations and rationale for conversion and maintenance of sinus rhythm. 1450 50

The aim of this study was to assess the impact of stroke volume (SV) on mitral annular velocities derived from tissue Doppler imaging (TDI). To this end, conventional echocardiographic variables and TDI derived mitral annular velocities (S', E', A') were obtained in 14 patients (pts) with increased SV (due to primary mitral (n=12) (ISV group)), in 41 pts with reduced SV (due to ischemic (n=27) or dilated cardiomyopathy (n=9) or hypertensive heart disease (n=5) (RSV group)) and 29 asymptomatic controls with normal SV (CON group). Systolic (S') and early diastolic (E') mitral annular velocities were elevated in the ISV group in the comparison to the CON group, but were significantly reduced in the RSV group. Late diastolic annular velocities (A') did not differ between the ISV and the CON group, but were lowest in the RSV group. On simple linear regression analysis, SV was significantly related to S' (r=0.74, p<0.001), to E' (r=0.74, p<0.001) and to A' (r=0.43, p<0.01). On multiple regression analysis, SV was a stronger independent predictor of S' and E' than conventional systolic or diastolic echocardiographic variables. Thus, stroke volume has a significant impact on TDI derived systolic (S') and early diastolic (E') mitral annular velocities. This should be considered, when TDI is used in the evaluation of LV performance or in the estimation of filling pressures.
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PMID:Stroke volume and mitral annular velocities. Insights from tissue Doppler imaging. 1549 95

The main goal of current antihypertensive therapy is to achieve a lowering of intra-arterial pressure by various mechanisms. A plethora of data suggests that this reduces cardiovascular morbidity and mortality due to stroke, heart failure and to a lesser extent, ischemic heart disease. Early cardiac manifestations of chronic hypertension, left ventricular hypertrophy (LVH) and diastolic dysfunction (CHF-D) confer additional risk of cardiovascular morbidity and mortality in patients with hypertension. Regression of left ventricular (LV) mass with antihypertensive therapy is associated with improved diastolic function and overall reduction in cardiovascular events, and this benefit may be independent of actual lowering of arterial pressure. Antihypertensive therapy should therefore be geared to both lower arterial blood pressure and specifically reverse pathophysiologic processes that promote LVH and CHF-D. Emerging therapies accomplish this without specifically affecting blood pressure. Therefore, future treatments for hypertension may require a combination of drugs performing complimentary tasks in lowering arterial pressure and reversing maladaptive physiologic and genetic processes causing hypertensive heart disease. This review summarizes the current and emerging approaches to the treatment of individuals with hypertensive heart disease.
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PMID:Antihypertensive drugs and the heart. 1617 92

Normal ejection fraction (EFs) is often equated with normal systolic function. However, midwall mechanics reveal systolic dysfunction in hypertensive heart disease accompanied by hypertrophic remodeling. Midwall mechanics are unstudied in patients with acute diastolic heart failure (HF). This study analyzed left ventricular (LV) midwall stress-shortening relations in 61 patients aged >60 years with hypertensive heart disease, HF, and normal EF. Sixty-one hypertensive patients (mean age 78 +/- 10 years) who presented with HF, each with an EF >50%, underwent echocardiography. Midwall mechanics were compared with those of 79 controls (mean age 75 +/- 8 years) without structural heart disease. Relative wall thickness (0.63 +/- 0.11 vs 0.46 +/- 0.10 mm) and LV mass (237 +/- 67 vs 177 +/- 57 g) were significantly greater in patients with HF compared with controls. Mean EFs were similar in patients with HF and controls (64 +/- 9% vs 67 +/- 9%). Although mean endocardial fractional shortening (35 +/- 7% vs 37 +/- 7%) was not significantly different, midwall shortening in patients with HF was significantly less compared with controls (16 +/- 2% vs 19 +/- 3%, p <0.05). Eighteen of the 61 patients with HF (30%) had midwall shortening that was <95% confidence intervals of the normal midwall stress-shortening relations. By this criterion, these patients had systolic dysfunction despite normal EF; they had smaller LV chambers (in dimension and volume), greater relative wall thickness, and smaller stroke volumes. In conclusion, almost 1/3 of patients hospitalized with diastolic HF had systolic dysfunction, characterized by abnormal midwall stress-shortening relations.
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PMID:Analysis of left ventricular systolic function using midwall mechanics in patients >60 years of age with hypertensive heart disease and heart failure. 1625 2

Other than age, left ventricular hypertrophy (LVH) is the most potent predictor of adverse cardiovascular outcomes in the hypertensive population, and is an independent risk factor for coronary heart disease, sudden death, heart failure and stroke. Although directly related to systolic blood pressure, other factors including age, sex, race, body mass index and stimulation of the renin-angiotensin-aldosterone and sympathetic nervous systems play an important role in the pathogenesis of LVH. LVH involves changes in myocardial tissue architecture consisting of perivascular and myocardial fibrosis and medial thickening of intramyocardial coronary arteries, in addition to myocyte hypertrophy. The physiologic alterations which occur as a result of these anatomical changes include disturbances of myocardial blood flow, the development of an arrhythmogenic myocardial substrate and diastolic dysfunction. The latter is directly related to the degree of myocardial fibrosis and is the hemodynamic hallmark of hypertensive heart disease. When diastolic dysfunction is present, left ventricular end-diastolic pressure increases out-of-proportion to volume and may be elevated at rest or with exertion leading to clinical heart failure. At least one third of heart failure patients in the United States can be considered to have heart failure related to diastolic dysfunction. Compared to heart failure patients with systolic dysfunction, diastolic heart failure patients are more likely to be older, female, and to be hypertensive at the time of presentation. Although it has been assumed that LVH may lead to systolic dysfunction, evidence is lacking that LVH resulting from hypertension is a major risk factor for systolic heart failure independent of coronary artery disease. Treatment of hypertension greatly attenuates the development of LVH and significantly decreases the incidence of heart failure. In patients with established LVH, regression is both possible and desirable and results in a significant reduction in adverse clinical endpoints.
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PMID:From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease. 1662 48

The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study provided extensive data on predisposing factors, consequences, and prevention of atrial fibrillation (AF) in patients with hypertension and left ventricular (LV) hypertrophy. Randomized losartan-based treatment was superior to atenolol-based treatment for reducing new-onset AF and complications, especially stroke, associated with new-onset or pre-existing AF. Potential mechanisms of AF prevention by angiotensin receptor blockade supported by LIFE results include greater reduction in left atrial size and LV hypertrophy. Differential effects of antihypertensive treatment on the left atrium and left ventricle may help prevent AF and reduce risk of stroke associated with hypertensive heart disease.
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PMID:The left atrium, atrial fibrillation, and the risk of stroke in hypertensive patients with left ventricular hypertrophy. 1912 45

Hypertension represents a complex, multifactorial disease and contributes to the major causes of morbidity and mortality in industrialized countries: ischemic and hypertensive heart disease, stroke, peripheral atherosclerosis and renal failure. Current pharmacological therapy of essential hypertension focuses on the regulation of vascular resistance by inhibition of hormones such as catecholamines and angiotensin II, blocking them from receptor activation. Interaction of G-protein coupled receptor kinases (GRKs) and regulator of G-protein signaling (RGS) proteins with activated G-protein coupled receptors (GPCRs) effect the phosphorylation state of the receptor leading to desensitization and can profoundly impair signaling. Defects in GPCR regulation via these modulators have severe consequences affecting GPCR-stimulated biological responses in pathological situations such as hypertension, since they fine-tune and balance the major transmitters of vessel constriction versus dilatation, thus representing valuable new targets for anti-hypertensive therapeutic strategies. Elevated levels of GRKs are associated with human hypertensive disease and are relevant modulators of blood pressure in animal models of hypertension. This implies therapeutic perspective in a disease that has a prevalence of 65million in the United States while being directly correlated with occurrence of major adverse cardiac and vascular events. Therefore, therapeutic approaches using the inhibition of GRKs to regulate GPCRs are intriguing novel targets for treatment of hypertension and heart failure.
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PMID:Regulation of GPCR signaling in hypertension. 2006 Aug 96

Clinical sequelae of hypertension include heart failure, arrhythmias, and ischemic events, especially myocardial infarction and stroke. Recognizing the hypertensive heart has diagnostic as well as prognostic implications. Current imaging techniques offer noninvasive approaches to detecting myocardial fibrosis, ischemia, hypertrophy, and disordered metabolism that form the substrate for hypertensive heart disease. In addition, recognition of aortopathy and atrial myopathy as contributors to myocardial disease warrant incorporation of aortic and atrial functional measurements into a comprehensive understanding of the hypertensive heart.
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PMID:The hypertensive heart. An integrated understanding informed by imaging. 2011 76

Hypertension (HTN) is the most common cause of non-traumatic ICH, yet echocardiography, which can stage hypertensive heart disease (HHD), is not part of the routine evaluation of patients with ICH. Previous studies have shown that angiotensin converting enzyme inhibitors and angiotensin receptor blockers are associated with regression of left ventricular hypertrophy (LVH) and reversal of myocardial fibrosis. Improvement in these architectural changes in the heart has been shown to improve outcomes and prevent major adverse cardiac events, including stroke. Obtaining echocardiography on ICH patients routinely could help to access the prevalence of HHD and to tailor antihypertensive regimens in this high risk group of patients. Further study is required to determine whether angiotensin directed therapies provide optimal secondary prevention in ICH patients with HHD.
Int J Stroke 2010 Oct
PMID:Is there a role for echocardiography in intracerebral haemorrhage? 2085 22

Although clinical cardiovascular outcomes, such as heart attack, stroke, and sudden cardiac death, have a dramatic onset, they result from prolonged exposure to an ever-growing array of risk factors. Several noninvasive procedures are available to assess the cumulative effect of these exposures with the goal of more precisely estimating a person's cardiovascular risk. These include ankle-brachial index, which provides an estimation of obstruction in major-vessel lumen caliber; carotid ultrasound, which evaluates carotid intima-media thickness and plaque, visibly quantifying atherosclerotic burden; aortic pulse wave velocity, which provides a measure of large-artery stiffness; and echocardiography, which measures left ventricular mass, providing a measure of subclinical hypertensive heart disease. In this narrative review, we discuss the role of each of these measures, with a particular emphasis on patients with chronic kidney disease.
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PMID:Surrogate markers of cardiovascular disease in CKD: what's under the hood? 2116 44


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