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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autonomic effect of various stimuli on haemodynamic variables is usually tested by changes in blood pressure (BP) and/or heart rate (HR). It is known that increased sympathetic drive of ventricles can interfere with repolarization process. This study was focused on reactive changes of maximal spatial T vector (sTmax), R-R and QTc intervals, in relation to BP changes in 79 boys and men, averaged age 17 +/- 2 years, 36 from them were adolescents with elevated BP (high normal or hypertension I according to WHO/ISH 1999) (ZTK), 19 normotensives (NTK), and 24 normotensive sportsmen. R-R, QTc intervals and maximal spatial T vector were recorded by a PC (Cardiag METE, Prague) with Frank lead system while sitting in mid-respiratory position, during mental arithmetic (MA), after handgrip and during passive head-up tilting to 60 degrees. BP was measured simultaneously by a cuff sphygmomanometer, using phases 1 and 5 of Korotkoff sounds. MA resulted in significant BP increase in all subgroups, however the reactive changes of systolic BP as well as magnitude of R-R shortening, sTmax decline were about two times higher, and in the case of QTc lengthening three times higher in sportsmen. Handgrip provoked in all subgroups in average the less reactive changes of diastolic BP, sTmax, R-R, and QTc intervals. Head-up tilting evoked in all subgroups a significant increase of diastolic BP that was again higher in sportsmen vs. ZTK and NTK. R-R intervals became significantly (p < or = 0.02) and more often shortened in sportsmen vs. ZTK and NTK. Relatively more evident decline of sTmax (more than 20%) in ZTK was the highest change from all observed parameters to all tested stimuli. Our results indicate that for analysis of effect stimuli, which modulate balance in autonomic nervous system, it is helpful to pay attention also to the parameters of repolarization process that may represent a sensitive indicator of sympathetic tonization in myocardial ventricles.
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PMID:[Effect of adrenergic stimuli on electrocardiographic and vectorcardiographic characteristics of ventricular repolarization]. 1274 40

The paper deals with hemorrhagic stroke (HS) pathogenesis and diagnosis in young people. Among cerebrovascular diseases in the young acute hemorrhagic strokes take noticeable place. Arterial hypertension, diabetes mellitus, smoking, alcoholism are among risk factors of subarachnoidal hemorrhage (SAH). Massive hemorrhages occur in the rupture of arterial aneurysms and arteriovenous malformations. HS in the young may be caused by blood diseases, i.e. leukemias, hemophilias, idiopathic thrombocytopenic purpura, coagulopathies; vasculitis in diffuse diseases of the connective tissue; non-inflammatory arteriopathies; drug addiction. Genetic predisposition to HS development is discussed with focus to such diseases as a family form of moya-moya disease, glucocorticoid-depressed hyperaldosteronism, elastic pseudoxanthoma, Marfan's syndrome, renal olycystosis, Sturge-Veber syndrome. It is recommended to use wider updated methods of neurovisualization (CT, MRT, angiography) in diagnosis of HS. The conclusion is made that HS diagnosis, especially in the young, needs a multidisciplinary approach with active participation of neurologist, neurosurgeon, therapist, endocrinologist, hematologist.
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PMID:[Specific features of pathogenesis and diagnosis of hemorrhagic stroke in young patients]. 1511 67

Adverse neurologic outcomes after cardiac surgery can have devastating consequences, among them increased mortality risk and, among survivors, loss of independence and a diminished quality of life. They also represent a burden on the health-care system, requiring prolonged hospitalizations and additional aftercare and, therefore, greater costs. Adverse outcomes are classified by their severity. Frank stroke is the most serious. This complication is associated with patient age; however, the presence of significant ascending aortic disease represents the greatest hazard. Multivariable analysis also indicates that prior neurologic events, diabetes, chronic obstructive pulmonary disease, preoperative status, and diffuse vascular disease are predictive. The second type of adverse cerebral outcome includes neurocognitive abnormalities such as memory loss and diminished emotional health. The strongest predictors of these abnormalities are hypertension and a history of alcohol use, as well as age. These predictive factors have been incorporated into the Multicenter Study of Perioperative Ischemia stroke-risk index, which clinicians can use to better assess the risk of adverse neurologic events. Clinical research examining the relationship between the predictive variables for neurologic adverse events and cerebral blood flow has suggested some surgical strategies for minimizing risk, such as limiting manipulation of the ascending aorta. The benefits of strategies such as using low or high mean arterial pressures and manipulating pump flow remain unclear. Off-pump coronary bypass surgery has been proposed as a means of reducing neurologic risk, but its effectiveness is unproved in this area. One pharmacologic strategy, the administration of aprotinin, has been shown to reduce the incidence of stroke in high-risk patients.
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PMID:Predicting and preventing adverse neurologic outcomes with cardiac surgery. 1649 92

One type of intrinsic response exhibited by the isolated and non-isolated heart is the well-known Frank-Starling mechanism, which endows the ventricles with performance characteristics such that the heart ejects whatever volume is put into it [heterometric autoregulation]. A second type of autoregulation in the isolated and no-isolated heart, one which apparently does not utilize the Frank-Starling mechanism, will be the main subject of this review. It requires at least a few beats to develop fully after an increase in activity. The ventricle then exhibits performance characteristics such that its end-diastolic pressure and fiber length tend to be maintained because of an increase in myocardial contractility. It will, therefore be referred to as homeometric autoregulation or Anrep effect. Assessment of ventricular load-independent parameters, including myocardial contractility, is important to better understand the pathophysiology of acute and right ventricular increased afterload. The role of the Anrep effect, in right ventricular dysfunction in patients with primary or secondary forms of pulmonary artery hypertension with chronic cor pulmonale, is analyzed and presented as an hypothesis to be considered in the pathophysiology in acute and in chronic states of right ventricular afterload.
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PMID:[Homeometric autoregulation in the heart. The Anrep effect. Its possible role in increased right ventricular afterload pathophysiology]. 1836 Oct 80

We report on a 78-year-old woman patient with macrothrombocytopenia with leukocyte inclusions (MTCP, May-Hegglin anomaly/Sebastian syndrome), who had no history of hemorrhagic symptoms and had a platelet count of 10,000 or less, but had a cerebral infarction. The patient was found to have idiopathic thrombocytopenic purpura, hypertension, and atrial fibrillation 16 years ago, yet received no medication. She was found to have had a cerebral infarction with aphasia as the chief complaint and was admitted to our hospital. Thrombocytopenia was found in three family members. Blood examinations revealed normal bleeding time and platelet aggregation ability. The patient was found to have the triad of giant platelets, thrombocytopenia, and inclusion bodies in leukocytes. Genetic analysis showed a mutation of the MYH-9 gene in the patients second daughter. Consequently, this patient received a diagnosis of MTCP. There have only been a few reports of the onset of thrombosis in patients with MTCP and no reports of the onset of cerebral infarction. Our report is the first case of MTCP in a patient with cerebral infarction.
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PMID:Cerebral infarction in a patient with macrothrombocytopenia with leukocyte inclusions (MTCP, May-Hegglin anomaly/Sebastian syndrome). 1878 Oct 47

QT interval is prolonged in hypertensive individuals, although the factors responsible for this increase are not completely understood. We questioned whether enhanced left ventricular mass (LVM) or increased systemic blood pressure represents the principal factor determining QT prolongation in the period of development of hypertension and left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR). In 12-and 20-week-old SHR (SHR12 and SHR20) and age-matched normotensive Wistar-Kyoto rats (WKY12 and WKY20), arterial systolic blood pressure (sBP) was measured using tail-cuff technique. Orthogonal Frank ECG was registered in anaesthetized animals in vivo, and bipolar ECG was measured in spontaneously beating isolated hearts in vitro. Progressive increase of sBP and LVM resulted in significant QT prolongation in SHR20 as compared to WKY12, WKY20, and also to SHR12 in vivo (WKY12: 82 +/- 9 ms, WKY20: 81 +/- 9 ms, SHR12: 88 +/- 15 and SHR20: 100 +/- 10, respectively; p < 0.05) but not in isolated hearts (WKY20: 196 +/- 39 ms and SHR20: 220 +/- 55, respectively; NS). In whole animals, QT duration was positively related to sBP (r = 0.6842; p < 0.001) but not to LVM (r = 0.1632, NS) in SHR20. The results suggest that QT prolongation in SHR developing hypertension and LVH depends on blood pressure rather than increase in LVM. In this period, myocardial hypertrophy is probably the predisposition for QT prolongation, but the significant change manifests only in the presence of elevated systemic factors.
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PMID:Prolonged QT interval is associated with blood pressure rather than left ventricular mass in spontaneously hypertensive rats. 1885 52

We performed on-pump coronary artery bypass graft surgery on a 54-year-old female, known case of chronic Idiopathic Thrombocytopenic Purpura (ITP), hypertension and dyslipidaemia who had presented to us with progressive exertional shortness of breath and chest pain. The decision of going on with CABG was made after two weeks of preoperative treatment with prednisolone. Her platelet counts pre-operatively and on the 4th post-operative day were 135 x 10(9)/L and 32 x 10(9)/L. She had an unremarkable post-operative recovery, without requiring whole blood or platelet transfusions. We recommend preoperative steroid treatment in patients with chronic ITP undergoing CABG.
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PMID:On pump coronary surgical revascularization in a patient with chronic immune thrombocytopenic purpura. 2022 90

The risk factors for haemorrhage in chronic idiopathic thrombocytopenic purpura (ITP) remain poorly understood. We classified 49 patients with chronic ITP into two groups on the basis of the presence (n = 11) or absence (n = 38) of hypertension and/or diabetes mellitus, and then analyzed their clinical and immunological characteristics. The patients with hypertension and/or diabetes were older than those without these complications. There were no significant differences between the two groups with regard to platelet count or the levels of platelet-associated immunoglobulin G, platelet-associated immunoglobulin M, and platelet-associated C3. Positivity for anti-glycoprotein IIb/IIIa and anti-glycoprotein Ib autoantibodies was also similar. However, severe purpura and a poor response to prednisolone were far more common in the patients with hypertension and/or diabetes. We conclude that ITP complicated by hypertension and/or diabetes may be resistant to prednisolone and thus require more careful treatment.
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PMID:Hypertension and diabetes mellitus increase the risk of haemorrhage in chronic idiopathic thrombocytopenic purpura. 2104 32

Heart failure is a clinical syndrome that results when the heart is unable to provide sufficient blood flow to meet metabolic requirements or accommodate systemic venous return. This common condition affects over 5 million people in the United States at a cost of $10-38 billion per year. Heart failure results from injury to the myocardium from a variety of causes including ischemic heart disease, hypertension, and diabetes. Less common etiologies include cardiomyopathies, valvular disease, myocarditis, infections, systemic toxins, and cardiotoxic drugs. As the heart fails, patients develop symptoms which include dyspnea from pulmonary congestion, and peripheral edema and ascites from impaired venous return. Constitutional symptoms such as nausea, lack of appetite, and fatigue are also common. There are several compensatory mechanisms that occur as the failing heart attempts to maintain adequate function. These include increasing cardiac output via the Frank-Starling mechanism, increasing ventricular volume and wall thickness through ventricular remodeling, and maintaining tissue perfusion with augmented mean arterial pressure through activation of neurohormonal systems. Although initially beneficial in the early stages of heart failure, all of these compensatory mechanisms eventually lead to a vicious cycle of worsening heart failure. Treatment strategies have been developed based upon the understanding of these compensatory mechanisms. Medical therapy includes diuresis, suppression of the overactive neurohormonal systems, and augmentation of contractility. Surgical options include ventricular resynchronization therapy, surgical ventricular remodeling, ventricular assist device implantation, and heart transplantation. Despite significant understanding of the underlying pathophysiological mechanisms in heart failure, this disease causes significant morbidity and carries a 50% 5-year mortality.
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PMID:The pathophysiology of heart failure. 2222 65

Antihypertensive treatment may reduce prolonged QT duration in hypertension. Generally, the reductions of blood pressure and/or of cardiac mass are believed to be the responsible factors. However, drugs are not equivalent in QT modulation despite similar antihypertensive and antihypertrophic action. We investigated the effect of a calcium channel blocker, lacidipine and an angiotensin-converting enzyme inhibitor, enalapril on QT duration in rats. Normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were treated with lacidipine (at the dose of 1.5 mg/kg per day for WKY and 3 mg/kg per day for SHR) or enalapril (5 mg/kg per day for WKY and 10 mg/kg per day for SHR) during 8 weeks. Tail-cuff systolic blood pressure (sBP), left ventricular weight (LVW), vascular function of isolated aorta and mesenteric artery and duration of QT (and QTc) interval on Frank electrocardiograms were evaluated. As expected, untreated SHR showed elevated sBP, impaired vascular reactivity, increased LVW and prolonged QT when compared with WKY (p < 0.05). After treatment, both agents markedly improved vascular reactivity and reduced sBP in SHR (p < 0.05). Additionally, enalapril reduced LVW in both hypertensive (by 17%; p < 0.05) and normotensive rats (by 13%; p < 0.05) and, consequently, corrected QT duration in SHR. Interestingly, lacidipine also reduced LVW in SHR (by 9%; p < 0.05), but without influence on prolonged QT. Moreover, lacidipine had no effect on LVW in WKYs but prolonged their QT interval (by 10%; p < 0.05). In conclusion, lacidipine did not reverse a progressive prolongation of QT in SHR, despite sBP lowering and LVW reduction. Thus, the lowering of blood pressure and/or reduction of LVW are not sufficient per se to normalize ventricular repolarization in hypertensive cardiac disease. More likely, modulation of QT prolongation by antihypertensive drugs is a function of their complex action on blood pressure, vascular function, cardiac mass and on reflex neurohumoral activation.
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PMID:Discrepant regulation of QT (QTc) interval duration by calcium channel blockade and angiotensin converting enzyme inhibition in experimental hypertension. 2262 43


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