Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The water-salt equilibrium and the degree of endogenous intoxication (albumin fluorescence test) were examined in 60 patients with transurethral resection of the prostate (TURP), 40 of whom had ischemic heart disease (IHD). Body temperature, ECG, ST segment and echocardioscopy were daily monitored perioperatively in all patients. The results showed a lack of any pronounced changes in the water-salt equilibrium in TURP that lasted up to 1.5 hours and included big volumes of 5% glucose; they were also indicative of a lower postoperative binding albumin ability, which is normally most pronounced in patients with hyperthermia. As for the IHD patients, hyperthermia was found to be concurrent in them with the onset of ischemia of the myocardium and with its low contractive ability, which can be referred to as a significant factor in case of the above patients.
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PMID:[Effect of transurethral resection of the prostate on the state of patients with ischemic heart disease]. 1520 71

Injury to the myocardium disrupts geometric integrity and results in changes to intracardiac pressure, wall stress and tension, and the pattern of blood flow through the heart. Significant disruption to pump function results in heart failure which is defined in terms of symptoms: breathlessness and fatigue, signs of salt and water retention, and neurohormonal activation. This syndrome most commonly occurs in the context of injury due to ischaemic heart disease and dilated cardiomyopathy but because patients with congenital heart disease (CHD) are born with sometimes gross distortions of cardiac anatomy they too are subject to the forces that drive heart failure. This paper explores the available data relating to the clinical and neurohormonal manifestations of heart failure in patients with congenital heart disease and describes how, by additionally exploring events at a cellular level, we may be able to arrive at a definition of heart failure relevant to this population.
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PMID:Towards defining heart failure in adults with congenital heart disease. 1559 75

Several international studies from Spain, the Netherlands, Poland, Croatia, and Finland indicate contradicting findings regarding cardiovascular dysfunction among seamen, deep sea fishermen, and harbor workers. The purpose of the present survey was to evaluate the prevalence of hypertension in a selected group of Lithuanian seamen. The survey was conducted during a one year period and involved sailors from commercial, passenger, and fishing boats. The survey took into account the sailors' marital status, education, professional rank and duty, and length of stay at sea. It also included demographical data, complete family health history, the sailor's awareness about their health in general, and awareness about their blood pressure in particular. Their dietary habits, changes in body weight, the history of alcohol intake and tobacco usage were also recorded. Analysis of our data indicates that 44.9% of Lithuanian mariners suffer from a clinically significant elevation of blood pressure, as compared to 53% of the general population of Lithuania. Some of the leading risk factors are: a high cholesterol diet and increased body mass index (BMI), smoking, alcohol abuse, family situation and level of education. The high prevalence of the cardiovascular risk factors was to be found related to ischemic heart disease and cerebrovascular illness. This may be influenced by poor eating habits, poor health awareness and other social and environmental factors which are common to seamen. Increased blood pressure is a widespread condition that affects a large portion of the population in developed countries. It is an important risk factor for cardiovascular and cerebrovascular disease, as well as a significant preventable cause of mortality. According to the World Health Organization (WHO), hypertension is a risk factor for cardiovascular disease, which accounts for an estimated 17 million deaths each year. With hypertension, the risk of stroke increases 2.6-3.8 times, the risk of ischemic heart disease (IHD)--2.0-2.2 times, and that of congestive heart failure (CHF)--3.0-4.0 times. Hypertension is often accompanied by other cardiovascular risk factors such as dyslipidemia, smoking, diabetes and increased body mass index (BMI). When hypertension is present in conjunction with other risk factors, the risk of mortality associated with IHD can increase tenfold. On the other hand, risk factors such as an increased BMI, smoking, alcohol abuse, lack of exercise and a diet high in salt and fatty foods can themselves play an instrumental role in the etiology of hypertension. Several studies have been performed on the prevalence of hypertension among the general population in Lithuania, which is higher than that of most other European countries. Reviews performed by the programs CINDI (Countrywide Integrated Noncommunicable Disease Intervention) and MONICA (MONItoring CArdiovascular Disease) determined that about half of all studied persons of middle age in Lithuania were hypertensive. Our work is the first study seeking to examine the prevalence of hypertension among Lithuanian seamen, as well as its association with various risk factors and dependence on demographic indices.
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PMID:Prevalence of hypertension in Lithuanian mariners. 1563 17

Chronic pain in the elderly is frequently a result of arthritic disorders, particularly osteoarthritis. The cyclo-oxygenase (COX)-2 inhibitors are as effective as standard NSAIDs for the relief of pain and for improving function in elderly patients with osteoarthritis and rheumatoid arthritis. COX-2 inhibitors increase the risk of serious gastroduodenal adverse reactions but there is evidence that they carry a lower risk for these adverse effects than standard NSAIDs, except when there is concurrent aspirin use. Since gastroduodenal disorders are the most frequently reported serious adverse effects of NSAIDs and these disorders occur more frequently in the elderly, COX-2 inhibitors offer an alternative to standard NSAIDs in this age group. However, they are not appropriate for many patients with cardiovascular and renal disease. The adverse reaction profile of the COX-2 inhibitors has confirmed the role of the COX-2 enzyme in renal function, salt and water homeostasis and the vascular endothelium. Thus, like standard NSAIDs, COX-2 inhibitors can cause renal failure, hypertension and exacerbation of cardiac failure. Of note is that these disorders are dose related. Thus, there are good reasons to avoid high doses of COX-2 inhibitors in the elderly. Clinical trials indicate that daily doses of rofecoxib 12.5 mg, celecoxib 100-200 mg, valdecoxib 10mg and etoricoxib 60 mg are the minimum effective doses of these agents. Data from the New Zealand Intensive Medicines Monitoring Programme indicate that celecoxib 200 mg/day and rofecoxib 25 mg/day are/were the most commonly prescribed doses and that 6% of patients had taken rofecoxib 50 mg/day for longer than recommended. Recent research indicates that COX-2 inhibitors have a thrombotic potential, especially in high doses and when use is prolonged, and this further limits the extent to which they can be used in the elderly. Important interactions with COX-2 inhibitors in the elderly include those with warfarin, which can result in loss of control of anticoagulation, and those with ACE inhibitors, angiotensin II type 1 receptor antagonists and diuretics, which can result in loss of control of blood pressure and cardiac failure and, in hypovolaemic conditions, renal failure. The clinical significance of an interaction between celecoxib and aspirin to reduce the antiplatelet effect of the latter drug is unknown. Preliminary information from spontaneous reporting systems indicates that there may be differences in the risk of cardiac failure and hypertension between standard NSAIDs and COX-2 inhibitors and between rofecoxib and celecoxib. More formal studies using equivalent doses are needed to test this observation. Use of COX-2 inhibitors may be considered in the elderly to reduce the risk of gastroduodenal complications associated with standard NSAIDs but only when consideration has first been given to use of less toxic medicines as alternatives or supplements, the appropriate dose of the COX-2 inhibitor or standard NSAID, the presence and possible impact of co-morbidities, and the implications of taking COX-2 inhibitors with any concomitant medications. Equally important is regular monitoring of the patient taking a COX-2 inhibitor for efficacy and adverse effects, and ensuring that the patient has a continuing need to keep taking the drug. Close attention also needs to be paid to intercurrent illnesses and new prescriptions that may reduce the safety of the COX-2 inhibitor. A standard NSAID plus a proton pump inhibitor may be equally effective as a COX-2 inhibitor in reducing the risk of gastroduodenal toxicity and if used the same prescribing advice applies. Current knowledge concerning the thrombotic potential of COX-2 inhibitors suggests that this combination, if tolerated, may be preferable to a COX-2 inhibitor, particularly where prolonged use is required. This knowledge also indicates that for patients with or at high risk of ischaemic heart disease or stroke, COX-2 inhibitors are contraindicated.
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PMID:Cyclo-oxygenase-2 inhibitors: when should they be used in the elderly? 1581 52

A reduction of coronary flow reserve has been reported in patients with hypertensive heart disease (HHD), which suggests that myocardial ischemia may contribute to the progression to cardiac failure in HHD. Therefore, we evaluated whether fibroblast growth factor (FGF)-2 and/or heparin, which induce angiogenesis, may affect cardiac function in the setting of HHD. We used Dahl salt sensitive (DS) rats as an HHD model. Direct intramyocardial injection of 100 microg of FGF-2 plus 1.28 microg of heparin (n = 6), 100 microg of FGF-2 (n = 6), 1.28 microg of heparin (n = 6) or saline (n = 6) were performed in 9-week-old rats. Echocardiography was performed to evaluate cardiac function at 9, 11, and 13 weeks of age. Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations were measured at 8 and 13 weeks of age. DS rats were killed 4 weeks after myocardial injection (at 13 weeks of age), and myocardial capillary density was assessed by von Willebrand factor staining. Injection of FGF-2 plus heparin significantly decreased left ventricular end-diastolic diameter (P < 0.0001) and left ventricular end-systolic diameter (P < 0.0001), significantly improved the reduction of left ventricular fractional shortening (P = 0.0005), significantly decreased plasma ANP (P < 0.0001) and BNP (P = 0.016) concentrations, and significantly increased myocardial capillary density (P = 0.0002) compared with injection of saline. These findings indicate that intramyocardial injection of FGF-2 plus heparin suppresses the progression of cardiac failure in DS rats. FGF-2 plus heparin administration may be a new therapeutic strategy for the treatment of HHD.
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PMID:Intramyocardial injection of fibroblast growth factor-2 plus heparin suppresses cardiac failure progression in rats with hypertensive heart disease. 1587 12

Many randomized trials have shown that a reduction in salt intake lowers blood pressure in hypertensive individuals. However, few have looked at the effects according to hypertension category. A recent analysis of the third and fourth National Health and Nutrition Examination Survey suggests that salt intake may not be related to blood pressure in isolated systolic or combined hypertension. To look at this further, we reanalyzed the data of our previous salt reduction trials. Hypertensive individuals were studied in randomized double-blind crossover studies: 1 month of usual salt intake compared with 1 month of reduced salt intake. In isolated systolic hypertension (n=24), blood pressure was reduced from 166+/-19/86+/-7 to 156+/-20/85+/-7 mm Hg (systolic P<0.001; diastolic P=0.459) with a reduction in urinary sodium from 175+/-51 to 87+/-38 mmol per 24-hour period (10.3 to 5.1 g per day of salt). In combined hypertension (n=88), blood pressure was reduced from 161+/-16/100+/-9 to 154+/-17/96+/-9 mm Hg (P<0.001) with a reduction urinary sodium from 176+/-65 to 98+/-51 mmol per 24-hour period (10.4 to 5.8 g per day of salt). These results demonstrate that salt reduction has a significant effect on blood pressure in isolated systolic and combined hypertension. The fall in systolic observed in isolated systolic hypertension would be predicted to reduce stroke by approximately one third, ischemic heart disease by one quarter, and heart failure by one quarter in the population between 60 and 80 years of age, in whom isolated systolic hypertension is the predominate form of hypertension and carries the highest risk. These results provide strong support for universal salt reduction in all hypertensives.
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PMID:Modest salt reduction lowers blood pressure in isolated systolic hypertension and combined hypertension. 1595 12

The link between endothelial nitric oxide synthase (eNOS) activation and vascular diameter during ischemia-reperfusion was investigated in the rat heart. After short (<30 min) and long (>45 min) time of ischemia conferred by coronary artery occlusion of the rats, reperfusion caused dilatation and constriction of arterioles, respectively. Partial oxygen pressure (pO2) measurement of the heart by the electrode confirmed the hyper-perfusion and no-reflow phenomena during reperfusion, as well as myocardial ischemia. The vascular diameter was correlated with phosphorylation of Akt and serine 1177 residue of eNOS, and formation of NO-bound guanylate cyclase (GC) by immuoflorescence study. Western blotting confirmed the phosphorylation of eNOS-Ser1177 depending on ischemia time. The constriction during reperfusion after 45 min of ischemia is supposedly caused by the inhibition of Akt-mediated eNOS-Ser1177 phosphorylation, which was suppressed by a PKC inhibitor chelerythrine, or ROS scavengers N-2-mercaptopropionyl glycine (MPG) and 4,5-Dihydroxy-1, 3-benzenedisulfonic acid disodium salt (Tiron). However, an endothelin receptor antagonist BQ123 alleviated the vasoconstriction by increasing NO availability but not eNOS-Ser1177 phosphorylation. Thus, vascular patency is correlated with eNOS-Ser1177 phosphorylation in association with ROS, and PKC during reperfusion. Endothelin inhibits vasodilatation by reducing NO availability during reperfusion.
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PMID:Endothelial NO Synthase (eNOS) phosphorylation regulates coronary diameter during ischemia-reperfusion in association with oxidative stress. 1603 23

Long-term administration of vasodilators increases shear stress, which is thought to be important for vascular growth in the heart. Nicorandil, an activator of ATP-sensitive potassium channels with a nitrate-like action, is a potent vasodilator. We have now investigated the effects of nicorandil on vascular growth and gene expression in the failing heart of Dahl salt-sensitive (DS) hypertensive rats. DS rats fed a high-salt diet from 6 weeks of age develop concentric cardiac hypertrophy secondary to hypertension at 11 weeks, followed by heart failure at 18 weeks. DS rats on such a diet were treated with a nonantihypertensive oral dose of nicorandil (6 mg/kg per day) or vehicle from 11 to 18 weeks of age. Treatment of DS rats with nicorandil improved cardiac function and attenuated the development of heart failure. Myocardial capillary and arteriolar densities did not differ between vehicle-treated DS rats and age-matched controls. The abundance of mRNAs for endothelial NO synthase (eNOS), vascular endothelial growth factor (VEGF), the VEGF receptor Flt-1, and basic fibroblast growth factor (bFGF) in the myocardium was markedly reduced in vehicle-treated DS rats compared with controls. Treatment of DS rats with nicorandil greatly increased capillary and arteriolar densities and inhibited the downregulation of eNOS, VEGF, fms-like tyrosin kinase-1, and bFGF gene expression. This, nicorandil stimulates coronary capillary and arteriolar growth and thereby likely suppresses the development of heart failure in DS rats. Nicorandil may prove beneficial for the treatment of hypertensive heart failure as well as of ischemic heart disease.
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PMID:Nicorandil promotes myocardial capillary and arteriolar growth in the failing heart of Dahl salt-sensitive hypertensive rats. 1617 16

The calcium channel blockers have emerged as important therapeutic modalities in the treatment of hypertension, ischemic heart disease, and other cardiovascular diseases. More recently, their potential benefit in recipients of organ transplants has come under closer scrutiny. Calcium channel blockers depress in vitro cellular immunity in an additive fashion with cyclosporine and have been demonstrated to reduce the incidence of rejection posttransplantation in early clinical trials. This class of drugs may also diminish ischemic damage to transplanted organs and reduce the destructive aspects of reperfusion injury. Because of their ability to depress cellular immune responses to mitogens, calcium channel blockers may also prove useful in decreasing the incidence of first-dose side effects (related to lymphocyte stimulation) in response to treatment with the OKT3 monoclonal antibody, a commonly used antirejection medication. Recent investigative efforts also suggest that calcium channel blockers may minimize cyclosporine nephrotoxicity by antagonizing either the direct or indirect vasoconstrictive actions of the drug. Some of the calcium channel blockers also reduce cyclosporine metabolism and excretion, thus allowing adequate levels of cyclosporine in blood with reduced doses of this valuable immunosuppressive agent. Cyclosporine-treated renal transplant recipients are frequently hypertensive, which is likely related to a salt-sensitive physiology. Calcium channel blockers have demonstrated important efficacy in reducing blood pressure in low-renin, salt-sensitive patients and similarly have been efficacious in controlling blood pressure in cyclosporine-treated transplant recipients. The numerous potential applications of calcium channel blockers in the field of organ transplantation illustrates the need for expanded clinical trials evaluating their use in this area.
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PMID:Calcium channel blockers in organ transplantation: important new therapeutic modalities. 1698 75

Hypertensive left ventricular hypertrophy (LVH) co-exists frequently with ischaemic heart disease. While ischaemic preconditioning (IPC) is known to protect against ischaemia-reperfusion injury in LVH, it is not known if other cardioprotective manoeuvres are effective. Bradykinin, a key autacoid mediator in IPC, is protective in normal hearts but its ability to protect against ischaemia-reperfusion injury in LVH is unknown. Hypertensive LVH was induced in male rats by 4 weeks treatment with deoxycorticosterone acetate (DOCA) and salt drinking fluid. Hearts were Langendorff perfused, subjected to 35 min coronary artery occlusion and 120 min reperfusion, and infarct size (AN/RZ %) was determined by tetrazolium staining. The effects of IPC with 2 x 5 min cycles of global ischaemia or 10 min pretreatment with bradykinin were assessed. DOCA-salt rats were markedly hypertensive and left ventricle/body weight ratio was 26% greater than in normotensive controls. Baseline coronary flow and risk zone/LV ratio were similar in normotensive hearts and DOCA-salt hearts, and infarct size was similar (AN/RZ 50.6+/-3.2% and 47.0+/-3.1%, respectively). IPC was equally protective in normotensive and DOCA-salt hearts (AN/RZ 18.6+/-3.3% and 18.4+/-2.3%, respectively, P < 0.01 versus corresponding control). Bradykinin 0.1, 0.2 or 0.5 microM pretreatment produced concentration-dependent infarct limitation in normotensive hearts (bradykinin 0.5 microM AN/RZ, 9.5+/-3.6%, P < 0.01 versus normotensive control), but the effect in DOCA-salt hearts was attenuated (bradykinin 0.5 microM AN/RZ, 23.4+/-3.8%). Further, the pre-ischaemic coronary vasodilator response to bradykinin was abrogated in DOCA-salt hypertensive hearts. We conclude that the cardioprotective action of bradykinin is markedly attenuated in moderate LVH and coronary vasodilator effect is lost. The reasons for reduced sensitivity to bradykinin in the hypertensive heart are unknown but these findings may have implications for the application of preconditioning-mimetic interventions in LVH.
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PMID:Attenuated cardioprotective response to bradykinin, but not classical ischaemic preconditioning, in DOCA-salt hypertensive left ventricular hypertrophy. 1707 63


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