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

A 68-year-old woman with idiopathic thrombocytopenic purpura (ITP) was admitted to our hospital with acute myocardial infarction on 7 February 1999. She had been treated since 1991 for mitral stenosis and regurgitation, atrial fibrillation due to mitralism, diabetes mellitus, hypertension, hyperlipidemia. Chest radiograph on admission showed cardiomegaly with congestion and cardiothoracic ratio was 63%. The platelet count on admission was 22,000/microliter, but she did not have petechia or purpura. Urgent coronary angiography revealed total occlusion in segment 7, and 13 and 75% stenosis in segment 4PD, 9 and 10. Subsequently, direct percutaneous transluminal coronary angioplasty (PTCA) was performed in segment 7. Dissection occurred during the intervention, and a coronary stent was implanted, we started heparin infusion and medication with ticlopidine hydrochloride as post-stenting therapy after the intervention, and there was no bleeding tendency.
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PMID:[A case of intracoronary stent implanted for acute myocardial infarction in an elderly patient with idiopathic thrombocytopenic purpura]. 1185 81

Late cardiovascular complications after operative repair of coarctation of the aorta include systemic hypertension, premature coronary artery disease, aortic valve abnormalities, aortic aneurysm, and recoarctation. We report the outcome in 274 subjects greater-than-or-equal50 years after coarctation repair. Operative repair of simple coarctation was performed on 274 patients at the University of Minnesota Hospital between 1948 and 1976. Twenty patients (7%) died in the immediate postoperative period. Of the 254 survivors, 2 were lost to follow-up, 45 (18%) died at a mean age of 34 years, and 207 (81%) were alive greater-than-or-equal50 years after the original operation. Coronary artery disease and perioperative deaths at the time of a second cardiac operation accounted for 17 of the 45 late deaths. Predictors of survival were age at operation and blood pressure at the first postoperative visit. Of the 207 long-term survivors, 92 (48%) participated in a clinical cardiovascular evaluation. Thirty-two of the 92 subjects had systemic hypertension that was predicted by age at operation, blood pressure at the first postoperative visit, and paradoxic hypertension at operative repair. New cardiovascular abnormalities detected at follow-up evaluation included evidence of a previous myocardial infarction, cardiomyopathy, atrial fibrillation, moderate to severe left ventricular outflow tract obstruction, moderate aortic valve regurgitation, recoarctation, and ascending aortic dilation. Thus, long-term survival is significantly affected by age at operation, with the lowest mortality rates observed in patients who underwent surgery between 1 and 5 years of age. More than 1/3 of the survivors developed significant late cardiovascular abnormalities.
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PMID:Long-term follow-up of patients after coarctation of the aorta repair. 1186 38

In 1979, we first reported occurrence of biventricular hypertrophy in the original normotensive Wistar-Kyoto (WKY) strain obtained from the National Heart, Lung, and Blood Institute, which was derived directly from the Kyoto laboratory of Okamoto. At that time, we recommended that both ventricles be weighted when WKY are studied so that invalid conclusions are not made. Because no paper confirmed these findings for almost 20 years, heart weights were reported in only a few WKY studies, and the cause of this biventricular hypertrophy remained unknown, we re-evaluated this problem in commercially available rats. We, therefore, investigated WKY rats using transthoracic echocardiography to define the congenital heart defect. Up to 28% of commercially available WKY rats demonstrated severe congenital cardiac abnormalities associated with biventricular hypertrophy. Ventricular septal defect with pulmonary regurgitation was the most commonly encountered cardiac defect; other abnormalities included patent ductus arteriosus, and valvular defects. Pathologic and invasive hemodynamic studies confirmed these echocardiographic findings. Because this defect occurs in a large number of WKY rats obtained commercially from 2 different sources, investigators using this strain must carefully measure both ventricular weights to be certain that inappropriate and invalid conclusions are not derived therefrom.
Hypertension 2002 Aug
PMID:High rate of ventricular septal defects in WKY rats. 1215 9

Williams syndrome is a genetic disorder associated with characteristic facies, supravalvar aortic stenosis, peripheral pulmonary stenosis, mental retardation, hypertension, premature aging of skin, and congenital cardiac defects. Many cardiac defects such as bicuspid aortic valve, mitral valve regurgitation, coarctation of the aorta, and ventricular or atrial septal defects are linked to the syndrome. Complete atrioventricular septal defect has rarely been associated with Williams syndrome and only one necropsy case has been reported in the literature. The long term follow up of Williams syndrome associated with complete atrioventricular septal defect is reported. During a 10 year follow up period, the pressure gradient in the ascending aorta did not increase despite narrowing of the ascending aorta as identified on an aortogram.
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PMID:Williams syndrome associated with complete atrioventricular septal defect. 1269 80

A 37-year-old male with mitral valve regurgitation presented for mitral valve replacement. He has been a C5 quadriplegic for 13 years. The patient had been discharged 2 months before to this admission after a complicated hospital course for Staphylococcus aureus infection of the left hip. His course was complicated by adult respiratory distress syndrome (ARDS) requiring prolonged intubation, acute renal failure (ARF) requiring dialysis, 10-day coma, and bacterial endocarditis now requiring mitral valve replacement. After initial stabilization with antibiotics and gradual improvement of the multiorgan system failure, the patient presented for valve replacement and worsening congestive heart failure (CHF). Para- and quadriplegic patients rarely undergo cardiac surgery requiring cardiopulmonary bypass (CPB). The explanation for this low incidence of heart surgery in this patient population ranges from physiologic changes from the spinal cord injury to their relatively short life span. Therefore, there is no vast knowledge of how these patients with spinal cord injury will physiologically respond to CPB. Chronic paraplegia presents unique anesthetic and perfusion challenges. General anesthesia for a patient with prolonged spinal cord damage can be difficult because of dysreflexia, muscle wasting, and potassium changes with depolarizing muscle relaxants. For the perfusionist, chronic paraplegia also accentuates hemodynamic responses to nonpulsatile flow with low peripheral vascular resistance common and difficult to treat. Dramatic increases in circulating catecholamine levels are a secondary result of the initiation of CPB that can cause a hypo- and hypertensive state. Depending on the level of spinal cord injury, one might expect acute hypo- or hypertension with the various phases of open-heart surgery and CPB. A viscous circle may occur because the hypertensive state is exaggerated because of inhibitory signals not passed below the spinal cord lesion and, therefore, the vasoconstrictive reflex continues unabated. The attack usually occurs abruptly and can lead to cerebrovascular hemorrhage and death if not controlled. Fortunately, we found this patient did not develop mass autonomic dysreflexia and was not difficult to wean from CPB. The problems associated with spinal cord injury present potential complications to this patient population. Numerous triggering mechanisms may lead to a variety of clinical complications. Consideration of a response/ treatment management plan for potential problems must be exercised by the surgical team.
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PMID:Unique considerations for the spinal cord injured patient undergoing cardiac surgery utilizing cardiopulmonary bypass. 1465 26

A 50-year-old man with a heart murmur from early childhood and a one year history of general fatigue was admitted. Cardiac examination showed a left ventricular-right atrial (LV-RA) communication, and aortic and mitral valve regurgitation (III/IV). At surgery, the LV-RA communication was located in the atrioventricular membranous portion 3 mm above the septal leaflet of the tricuspid valve. The etiology of the LV-RA communication was congenital and valvular diseases were acquired changes caused by sclerosis due to infected endocarditis or hypertension. The diameter of the LV-RA communication defect was 6 mm, and the fibrous tissue around the defect was closed directly. Next, double-valve replacement was performed safely. However, the day after surgery, the patient developed complete atrioventricular block and implantation of a DDD pacemaker was required. He was discharged without other complication. We recommend the careful closure of the LV-RA communication defect, if the defect is small and rich in fibrous tissue.
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PMID:[Surgical treatment of left ventricular-right atrial communication complicated with aortic and mitral valves regurgitation: report of a case]. 1497 6

Mild-to-moderate aortic and mitral regurgitation are frequently detected by echocardiogram in asymptomatic hypertensive patients. Our goal was to assess the prevalence and impact of mild-to-moderate mitral and/or aortic regurgitation on left ventricular (LV) structure and function in patients with hypertension and LV hypertrophy (LVH). Hypertensive patients with ECG LVH enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy were evaluated. Among 939 patients with needed LV measurements and Doppler data, 242 had mild (1+) valvular regurgitation, and 51 patients had moderate (2+ or 3+) regurgitation of one or both valves. In analyses adjusting for gender, patients with mild mitral and/or aortic regurgitation had larger LV internal dimensions (5.25 vs 5.33 cm, P<0.05), higher LV mass indexed for body surface area (122 vs 125 g/m(2), P<0.05) or height(2.7) (55.4 vs 57.3, P<0.05), and larger left atrial diameter. Patients with moderate regurgitation of one or both valves had larger LV chambers (5.25 vs 5.9 cm, P<0.001), greater mean LV mass (232 vs 248 g, P<0.001) and LV mass indexed for body surface area or height(2.7), and higher Doppler stroke volume. Patients with moderate valvular regurgitation also had a higher prevalence of LVH due to an increased prevalence of eccentric LVH. There were no differences among groups defined by the presence and severity of valvular regurgitation in cardiac output, total peripheral resistance, or pulse pressure/stroke volume, indicating that the observed inter-group differences in LV geometry were not due to differences in the haemodynamic severity of hypertension. Hypertensive patients with mild-to-moderate mitral or aortic valvular insufficiency have additional LV structural and functional changes that may affect prognosis.
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PMID:Impact of valvular regurgitation on left ventricular geometry and function in hypertensive patients with left ventricular hypertrophy: the LIFE study. 1504 17

Diving with self-contained underwater breathing apparatus (scuba) has become a popular recreational sports activity throughout the world. A high prevalence of cardiovascular disorders among the population makes it therefore likely that subjects suffering from cardiovascular problems may want to start scuba diving. Although scuba diving is not a competitive sport requiring athletic health conditions, a certain medical fitness is recommended because of the physical peculiarities of the underwater environment. Immersion alone will increase cardiac preload by central blood pooling with a rise in both cardiac output and blood pressure, counteracted by increased diuresis. Exposure to cold and increased oxygen partial pressure during scuba diving will additionally increase afterload by vasoconstrictive effects and may exert bradyarryhthmias in combination with breath-holds. Volumes of gas-filled body cavities will be affected by changing pressure (Figure 1), and inert gas components of the breathing gas mixture such as nitrogen in case of air breathing will dissolve in body tissues and venous blood with increasing alveolar inert gas pressure. During decompression a free gas phase may form in supersaturated tissues, resulting in the generation of inert gas microbubbles that are eliminated by the venous return to the lungs under normal circumstances. Certain cardiovascular conditions may have an impact on these physiological changes and pose the subject at risk of suffering adverse events from scuba diving. Arterial hypertension may be aggravated by underwater exercise and immersion. Symptomatic coronary artery disease and symptomatic heart rhythm disorders preclude diving. The occurrence of ventricular extrasystoles according to Lown classes I and II, and the presence of atrial fibrillation are considered relative contraindications in the absence of an aggravation following exercise. Asymptomatic subjects with Wolff-Parkinson-White syndrome may be allowed to dive, but in case of paroxysmal supraventricular tachycardia they must refrain from diving. Pacemakers will fail with increasing pressure, but some manufacturers have proven their products safe for pressure equivalents of up to 30 m of seawater, so that patients may dive uneventfully when staying within the 0-20 m depth range. Significant aortic or mitral valve stenosis will preclude diving, whereas regurgitation only will not be a problem. Right-to-left shunts have increasingly gained attention in diving medicine, since they may allow venous gas microbubbles to spill over to the arterial side of the circulation enabling the possibility of arterial gas embolism. Significant shunts thus preclude diving. The highly prevalent patent foramen ovale is considered a relative contraindication only when following certain recommendations for safe diving (Table 2). Metabolic disorders are of concern, since adiposity is associated with both, higher bubble grades in Doppler ultrasound detection after scuba dives when compared to normal subjects, and an increased epidemiologic risk of suffering from decompression illness. In conclusion, cardiovascular aspects are important in the assessment of fitness to dive, and certain cardiovascular conditions preclude scuba diving. Any history of cardiac disease or abnormalities detected during the routine medical examination should prompt to further evaluation and specialist referral.
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PMID:[Scuba diving and the heart. Cardiac aspects of sport scuba diving]. 1524 40

In patients with superinvasion opisthorchiasis of prolonged invasion, 84% develop duodenal hypertension, 94% of the patients are found to have gastric hypertension; duodenogastric reflux with formation of chronic gastritis and reorganization is revealed in 75%. Reflux of gastric contents into the esophagus gives rise to chronic eosophagitis, regurgitation of intestinal contents into the pancreatic duct is a cause of chronic indurative pancreatitis of the head of the gland. In cases of duodenal hypertension, the rates of pancreatic O. felineus invasion are as high as 93.7%.
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PMID:[Duodenogastroesophageal reflux disease as a complication of superinvasion opisthorchiasis]. 1548 77

Comparison of the human cardiovascular system with arrangements of circulatory systems found in lower vertebrates and invertebrates allows appreciation of the functional elegance of our double circulation with systemic and pulmonary vascular trees served by a single looped and septated heart. In the pulmonary part of the circulation, consideration of the nature of alveolar microvessels in relation to the system as a whole may throw light on the pathophysiology of pulmonary regurgitation and pulmonary hypertension. Pulmonary microvessels impose remarkably little resistance to flow compared with the systemic. This may be attributed to their delicate, compliant structure, with tissue support on one side only, their respiratory walls remaining relatively free to expand in alveolar air. Low resistance may also depend on the branch pattern of alveolar capillaries, with almost immediate proximity between bifurcations and confluences in a uniquely dense, interconnected network. In the presence of free pulmonary regurgitation, pulmonary microvessels probably play a valve-like role, representing a low-resistance boundary or watershed between pulmonary arteries and veins. This microvascular watershed imposes little resistance to systolic forward flow, but in diastole, with venous pressures being kept low by function of the left heart, there is presumably little or no reversal of gradient to move blood back through the capillaries. The delicacy and potential vulnerability of alveolar capillaries to elevation of flow and pressure is likely, however, to go with a protective feedback circuit which, in abnormal circumstances, could contribute to development of arteriolar medial hypertrophy and pulmonary arterial hypertension.
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PMID:Pulmonary resistance in cardiovascular context. 1559 72


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