UMLS:C0022116 - FACTA Search

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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The number of an elderly patient who has hypertension with diabetes mellitus has been increasing year by year since the life style of people has become Americanized in our country. Metabolic syndrome is characterized by hypertension, dyslipidemia, central adiposity and insulin resistance. It is recently recognized as the high risk for the macrovascular disease such as cerebral infarction and acute myocardial infarction. In diabetic patients, to prevent the life-threatening event or slow complications intensive blood pressure control is as efficacious as good glycemic control. The optimal blood pressure level to reduce hypertension-related morbidity and mortality in diabetic elderly has been proposed 130/80 mmHg in JSH 2004. The blood pressure level in the elderly should be lowered very slowly with careful monitoring of systemic ischemia. Early use of antihypertensive drug combinations is gaining favor. As the first step therapy would be recommended angiotensin receptor blocker, angiotensin-converting enzyme inhibitor and sustained release calcium channel blocker. Especially in the elderly, good control of life-style related diseases would be achieved through a team effort comprising the clinician, psychologist, nurse, pharmacologist, dietitian, other professionals and the patient's family. Comprehensive geriatric assessment can facilitate the maintenance of drug compliance for well control of blood pressure level.
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PMID:[Management of hypertension with diabetes mellitus in the elderly]. 1594 90

Percutaneous coronary intervention (PCI) was introduced in 1977, to treat single, discrete lesions in patients with stable symptoms, and favorable anatomy. Increased operator experience and numerous technical advances, notably including bare-metal stents (BMS) and then drug-eluting stents (DES), and a number of adjunctive pharmacologic modalities, have allowed for the gradual application of PCI to far more diverse clinical and anatomic subsets. The proper role of PCI, compared with both medical therapy and coronary artery bypass graft (CABG) surgery, is evolving. This manuscript is synthesized from literature review of randomized clinical trials, and some cohort investigations, and 21 years of PCI experience, which has been focused on high-risk patients. Current American College of Cardiology/ American Heart Association/ Society for Cardiac Angiography and Interven-tions (ACC/AHA/ SCA&I) Guidelines, and most research, are based upon a perspective (conventional paradigm') that categorizes patients primarily based upon number of major' coronary (left anterior descending artery, circumflex and right) arteries with a >70% stenosis, and whether left ventricular function is normal or abnormal (left ventricular ejection fraction < or >0.50). This paradigm developed when: a) CABG was the only revascularization option, and b) medical therapy was quite limited. All of the trials demonstrating survival benefit with aspirin, clopidogrel, statins, angiotensin-converting-enzyme inhibition (ACE-I) or angiotensin receptor blockers (ARB), and beta-blockers; coupled with the PCI versus thrombolytics trials in ST-elevation myocardial infarction (STEMI), and non-STEMI strategy trials, both of which include revascularization almost exclusively by PCI, make this conventional paradigm, outdated and counterproductive. Attempts to compare CABG and PCI have de-emphasized their very different advantages and disadvantages. The new paradigm makes major division of patients based upon whether patients have stable or unstable: a) ischemia and b) hemodynamics, and c) whether they are having acute myocardial infarction (MI). The first issue to be settled is whether the patient is likely to benefit from revascularization. If little or no benefit can be envisioned, the patient should be managed medically. Unstable ischemia and unstable hemodynamics, and acute MI, all favor emergent or urgent revascularization. Clinical features, which generally favor PCI for revascularization, include hemodynamic instability, STEMI and non-STEMI; and severe comorbidity, particularly cerebral, pulmonary, or hepatic comorbidity. Anatomic features, which generally favor CABG, include unprotected left main stenosis, especially involving the bifurcation, one or more graftable chronic total occlusions (CTO), and bifurcation disease with large important side-branches. Old age and severely reduced left ventricular function are associated with higher risks, with either CABG or PCI. Small caliber and diffusely diseased vessels may imply lower expectation of success, by either CABG or PCI.
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PMID:Multivessel percutaneous coronary intervention: a new paradigm for a new century. 1617 81

The pharmacologic management of the patient post myocardial infarction (MI) aims to achieve several goals. Chief among these is to prevent subsequent events, which include death, reinfarction, and rehospitalization. Secondary goals include preventing arrhythmias, minimizing left ventricular (LV) remodeling, and preventing progression to heart failure. This review describes practical algorithms for use in the pharmacologic management of the patient post MI based on American Heart Association/American College of Cardiology guidelines. The intensity of drug treatment is determined guided by the degree of LV dysfunction and the presence or absence of ischemia and arrhythmic risk markers. All patients post MI require an angiotensin-converting enzyme (ACE) inhibitor and antiplatelet therapy, usually with aspirin. In individuals who cannot tolerate an ACE inhibitor, an angiotensin receptor blocker (ARB) is an adequate substitute. Numerous studies document the efficacy of ACE inhibitors, which decrease mortality and the risk of heart failure and stroke. Aldosterone blockade is recommended long-term for patients post MI with an LV ejection fraction < or = 40% and either symptomatic heart failure or diabetes. Use of a beta blocker is an important addition to most post-MI drug regimens. Beta blockers decrease mortality and are especially effective in patients with impaired LV function. Among the beta blockers, carvedilol, which also has alpha-adrenergic receptor blocking activity, was found to decrease mortality significantly in patients with low ejection fractions and heart failure. Another drug therapy of value in post-MI treatment is use of calcium-channel blockers. These are restricted to patients with conserved LV function in whom congestion is absent and in whom beta blockers are contraindicated. Current guidelines also recommend that patients post MI with elevated cholesterol levels should be prescribed lipid therapy with a statin at hospital discharge.
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PMID:Practical algorithms for pharmacologic management of the post myocardial infarction patient. 1645 Aug 10

The decision to offer patients with myocardial ischemia a coronary artery bypass graft (CABG) surgery has been largely determined by extent of coronary artery disease (CAD) and left ventricular function, since the early 1970's. Based upon subset analyses, and long-term follow-up, of three moderate-sized trials of stable patients and two small trials of unstable angina (excluding recent myocardial infarction, MI) patients, the notion has persisted that patients with left main narrowing >50% or three-vessel stenoses >70%, or even two-vessel stenoses >70%, where one of the vessels is the proximal left anterior descending, derive a "survival benefit" relative to medical therapy (MED), from CABG (anatomic paradigm). The MED of the original CABG versus MED trials consisted of little more than anti-anginal medications, used on an as-needed basis. In the ensuing 3 decades, multiple large, well done, randomized clinical trials have established a survival benefit for 4 different forms of MED among a broad spectrum of CAD patients. Aspirin; lipid lowering, especially with statins; b-blockers; and angiotensin-converting-enzyme inhibitors and/or angiotensin receptor blocking agents; have all been shown to enhance survival, as well as reduce other objective adverse outcomes of CAD. The advances in MED, coupled with the small but significant mortality and morbidities of both CABG and percutaneous coronary intervention (PCI), are among the reasons to skeptically consider potential "survival benefit" of revascularization. A more common and far more easily justified reason to consider revascularization is to relieve "medically refractory" myocardial ischemia, particularly when the ischemia is accompanied by symptoms. Accordingly, documentation of medically refractory myocardial ischemia provides the answer to the first question of myocardial revascularization, "Is this patient likely to derive clinical benefit from revascularization, at this time?" It is only after this question has been answered that one needs to consider the relative advantages and disadvantages of PCI versus CABG (physiologic paradigm). Two of the relative advantages of PCI, namely speed of reperfusion, and relatively low morbidity, are among the reasons that most randomized trial data, and most clinical application of revascularization to patients with MI (ST-elevation MI [STEMI], and non-STEMI) have been by PCI. In contrast, for stable patients with medically refractory ischemia, anatomic considerations continue to be relevant to the choice between CABG and PCI. Specific advantages of CABG include: its potential to revascularize chronically occluded vessels with collaterals supplying viable myocardium; the fact that conduits protect territories rather than simply treating lesions; and the greater durability of conduits compared to bare-metal stents (drug-eluting stents may change the picture). Based on these principles, physiologic, rather than anatomic, considerations are most useful in determining whether to revascularize, and how urgently to revascularize (STEMI is an emergent indication and high-risk non-STEMI an urgent indication). Coronary anatomy, including both number of vessels and lesion characteristics, continues to help decide between CABG and PCI, and in formulating patient specific strategies.
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PMID:PCI versus CABG versus medical therapy in 2006. 1701

Recent studies have shown that in response to vascular damage or ischemia, bone marrow-derived endothelial progenitor cells (EPCs) are recruited into the circulation. To investigate whether antihypertensive treatment has an influence on the number of circulating EPCs, patients with essential hypertension were treated either with the angiotensin receptor antagonist telmisartan, the calcium channel blocker nisoldipine, or their combination for 6 weeks. At baseline and after 3 and 6 weeks of treatment, EPCs were identified and quantified by fluorescence-activated cell sorting (FACS) analysis and by their capacity to generate colony-forming units of the endothelial lineage (CFU-EC) in a methylcellulose-based assay. During treatment, patients in the nisoldipine groups, but not in the telmisartan group, showed a significant mobilization of EPCs, which in part had the capacity to generate large-sized colonies comprising more than 1,000 cells. Moreover, a remarkable correlation between the number of CFU-EC and the number of circulating CD133(+)/CD34(+)/CD146(+) cells was observed, thereby providing strong evidence that cells with this phenotype represent functional EPCs. No correlation was found between the numbers of CFU-EC and the blood pressure levels at any time point during the treatment. Hence, nisoldipine-induced mobilization of EPCs might represent a novel mechanism by which this antihypertensive compound independently of its blood pressure-lowering effect contributes to vasoprotection in patients with essential hypertension.
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PMID:Mobilization of putative high-proliferative-potential endothelial colony-forming cells during antihypertensive treatment in patients with essential hypertension. 1752 Dec 43

Hypertension is a leading contributor to the burden of cardiovascular disease. The importance of lowering blood pressure (BP) to reduce the risk of cardiovascular events has been demonstrated in numerous clinical trials. Most patients require combination antihypertensive therapy utilizing agents from complementary drug classes to achieve BP goals. A calcium channel blocker (CCB)/angiotensin receptor blocker (ARB) combination is a rational approach for such an antihypertensive strategy. Benefits of CCB/ARB combination therapy include additive BP-lowering effects and lower incidences of adverse events (AEs). These agents demonstrate benefits associated with their respective drug classes. The ARBs confer stroke protection, renal protection, and tolerability similar to placebo, without dose-related symptomatic and metabolic AEs, while CCBs are beneficial in reducing stroke and treating angina and cardiac ischemia. The efficacy of this combination has been recently investigated in clinical trials wherein amlodipine was combined with olmesartan medoxomil or valsartan. This article discusses the rationale for using CCB/ARB combinations in patients with hypertension.
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PMID:Angiotensin receptor blocker and dihydropyridine calcium channel blocker combinations: an emerging strategy in hypertension therapy. 1933 60

Random pattern skin flaps are still widely used in plastic surgery. However, necrosis in the distal portion resulting from ischemia is a serious problem, increasing the cost of treatment and hospitalization. To enhance skin flap viability, a variety of pharmacologic agents have been intensively investigated. The aim of this study was to assess the effect of enalapril (an angiotensin-converting enzyme inhibitor) and losartan (an angiotensin receptor blocker) in skin flap viability. Male rats of 200 to 250 g were used. Different doses of enalapril (5, 20, and 50 mg/kg) and losartan (5 mg/kg) were administrated 30 minutes prior to elevate the flap. Flap survival area was evaluated on the seventh postoperative day. Enalapril improved survival area in a dose-dependent manner, but losartan failed to improve survival area, which suggested that the effect of enalapril was not mediated through AT1 receptors.
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PMID:The effect of enalapril on skin flap viability is independent of angiotensin II AT1 receptors. 1946 Dec 89

Hypertension is common and occurs in a majority of autosomal dominant polycystic kidney disease (ADPKD) patients before the loss of kidney function. Hypertension relates to progressive kidney enlargement and is a significant independent risk factor for progression to ESRD. The pathogenesis of hypertension in ADPKD is complex and dependent on many factors that influence each other. Pkd1 and Pkd2 expression levels are highest in the major vessels and are present in the cilia of endothelial cells and in vascular smooth muscle cells. Decreased or absent polycystin 1 or 2 expression is associated with abnormal vascular structure and function. Pkd1/Pkd2 deficiency results in reduced nitric oxide (NO) levels, altered endothelial response to shear stress with attenuation in vascular relaxation. Ten percent to 20% of ADPKD children show hypertension and the majority of adults are hypertensive before any loss of kidney function. Cardiac abnormalities such as left ventricular hypertrophy and carotid intimal wall thickening are present before the development of hypertension in ADPKD. The activation of the renin-angiotensin-aldosterone system occurs in ADPKD because of decreased NO production as well as bilateral cyst expansion and intrarenal ischemia. With increasing cyst size, further activation of the RAAS occurs, blood pressure increases, and a vicious cycle ensues with enhanced cyst growth and hypertension ultimately leading to ESRD. The inhibition of the angiotensin aldosterone system is possible with angiotensin converting enzyme inhibitors and angiotensin receptor blockers. However, interventional studies have not yet shown benefit in slowing progression to renal failure in ADPKD. Currently, large multicenter studies are being performed to determine the beneficial effects of RAAS inhibition both early and late in ADPKD.
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PMID:Hypertension in autosomal dominant polycystic kidney disease. 2021 18

An understanding of onco-cardiology or cardio-oncology is critical for the effective care of cancer patients. Virtually all antineoplastic agents are associated with cardiotoxicity, which can be divided into 5 categories: direct cytotoxic effects of chemotherapy and associated cardiac systolic dysfunction, cardiac ischemia, arrhythmias, pericarditis, and chemotherapy-induced repolarization abnormalities. Radiation therapy can also lead to coronary artery disease and fibrotic changes to the valves, pericardium, and myocardium. All patients being considered for chemotherapy, especially those who have prior cardiac history, should undergo detailed cardiovascular evaluation to optimize the treatment. Serial assessment of left ventricular systolic function and cardiac biomarkers might also be considered in selected patient populations. Cardiotoxic effects of chemotherapy might be decreased by the concurrent use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, or beta-blockers. Antiplatelet or anticoagulation therapy might be considered in patients with a potential hypercoagulable state associated with chemotherapy or cancer. Open dialogue between both cardiologists and oncologists will be required for optimal patient care.
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PMID:Cardio-oncology/onco-cardiology. 2118 56

Numerous studies have documented the association between endothelial dysfunction and adverse cardiovascular events. For example, coronary artery disease is associated with functional and structural changes of the coronary arteries, resulting in ischemia or plaque rupture, and is highly associated with endothelial dysfunction. Recent data suggest that implantation of drug-eluting stents (DES) can induce coronary artery endothelial dysfunction at follow-up when compared with bare-metal stents (BMS) and that this endothelial dysfunction may be associated with late stent thrombosis. Indeed, despite the superiority of DES in preventing restenosis, the incidence of death and myocardial infarction is similar when comparing DES with BMS. Medical treatment, such as statins, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers, can improve endothelial dysfunction. Thus, administration of these drugs along with percutaneous coronary intervention (PCI) may be a low-risk strategy to provide therapeutic benefit by stabilizing unstable plaque or by suppressing new lesion formation in patients undergoing PCI.
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PMID:Effect of coronary endothelial function on outcomes in patients undergoing percutaneous coronary intervention. 2139 93

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