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

The conceptual model of the classical "ischemic cascade" has served cardiologists well for decades. It correctly predicts clinical findings during imaging stress testing in the presence of coronary artery disease or epicardial coronary artery spasm, where perfusion and wall motion abnormalities provide a substantially higher sensitivity than ECG changes. However, empirical experience has taught us that stress-induced ischemic-like ECG changes, often accompanied by perfusion abnormalities, are the rule rather than the exception in pathophysiological conditions during which the occurrence of ischemia usually cannot be proven, characterized by angiographically normal arteries and reduced flow reserve, such as syndrome X, arterial hypertension and hypertrophic cardiomyopathy. These stress-induced "echocardiographically silent" ST segment changes may be associated with impaired coronary flow reserve and systemic endothelial dysfunction. In hypertrophic cardiomyopathy stress-induced ischemic-like ST segment depression is linked to higher long-term incidence of adverse events. It is entirely likely that our monolithic view of ischemia mirrored in the classical ischemic cascade should be integrated by the awareness of the reverse or alternative "ischemic" cascade best describing microvascular disease, with ECG changes coming first, perfusion abnormalities second, and echocardiographic changes usually being absent. Not all forms of myocardial ischemia are the same, and milder, patchy degrees of myocardial ischemia--as those hypothesized, but not proven, in microvascular angina--remain silent in its mechanical functional manifestations and may well represent a physiological scotoma of stress echocardiography. "Anatomic lies" on the ECG may be overturned into "physiologic truths" when coronary flow reserve or systemic endothelial function is considered.
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PMID:The alternative "ischemic" cascade in coronary microvascular disease. 1060 88

Acute myocardial ischemia, which results from a significant imbalance between myocardial oxygen demands and myocardial oxygen supply, occurs in as many as six million persons with atherosclerotic coronary artery disease in the United States. Accordingly, a clear understanding of the physiologic and pathophysiologic factors that influence coronary artery blood flow is important to the clinician and provides the basis for the judicious use of medications for the treatment of patients with atherosclerotic coronary artery disease. This review discusses the endothelial, metabolic, myogenic, and neurohumoral mechanisms of coronary blood flow regulation and the interaction of the different mechanisms in the regulation of coronary blood flow. The importance of nitric oxide in coronary blood flow regulation is emphasized. We also discuss the common clinical problems of hyperlipidemia and coronary atherosclerosis, coronary artery spasm, and systemic arterial hypertension that result in coronary artery endothelial dysfunction, the impaired production and increased inactivation of nitric oxide, and impairment in coronary blood flow regulation. This information is important to clinicians because more than forty million people in the United States have atherosclerotic or hypertensive heart disease and therefore are at risk for significant myocardial complications due to impairment of coronary blood flow regulation.
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PMID:Coronary artery blood flow: physiologic and pathophysiologic regulation. 1062 79

We compared the risk factors for coronary spasm with those for coronary atherosclerosis in 183 patients with coronary spasm, 132 patients with coronary organic stenosis, and 224 control subjects with chest pain syndrome. Our findings confirmed that, when compared with controls, age, gender, total cholesterol, LDL-cholesterol, hypertension, diabetes mellitus, and cigarette smoking are all significant risk factors for coronary organic stenosis. On the other hand, only cigarette smoking proved to be a significant risk factor for coronary spasm. Also, when compared between coronary spasm group and coronary organic stenosis group, the incidence of cigarette smoking in males was significantly higher in the coronary spasm group than in the coronary organic stenosis group. We conclude that cigarette smoking is a crucial risk factor for coronary spasm. On the other hand, serum lipid levels and the incidence of hypertension and diabetes mellitus were within the normal ranges in the coronary spasm patients and were thus poorly associated with coronary spasm. These results showed that the risk factors for coronary spasm differ significantly from those for atherosclerosis-based coronary stenosis in the Japanese. Among the risk factors for coronary atherosclerosis (organic stenosis) smoking alone was a significant preventable risk factor for coronary artery spasm.
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PMID:Comparison of the risk factors for coronary artery spasm with those for organic stenosis in a Japanese population: role of cigarette smoking. 1064 52

Although the pathogenic mechanisms involved in predisposing individuals to hypertension are not well defined, evidence is accumulating that suggests a strong genetic transmission. Animal studies and some clinical investigations have revealed that aberrant NO production may be an important contributing factor. Indeed, a missense mutation in the endothelial NO gene caused by a Glu298Asp alteration has been strongly associated with essential hypertension, coronary artery spasm, and myocardial infarction. Recently, another point mutation caused by a T-786-->C transition in the 5'-flanking region of the endothelial NO synthase gene has been identified and, like the Glu298Asp mutation, is associated with coronary artery spasm. The present study was conducted to determine the effect of the T-786-->C point mutation on hypertension. We investigated the interaction between the endothelial NO synthase T-786-->C polymorphism and blood pressure in a large (n=705) clinically healthy population. Allele frequencies for the T and C alleles were 62% and 38%, translating into 39%, 46% and 15% of the population having the T/T, T/C, and C/C genotypes, respectively, for the T-786-->C point mutation. Subjects with the C/C genotype had significantly higher systolic blood pressures and were 2.16(95% confidence interval, 1.3 to 3.7) more likely to be hypertensive. Therefore, the -786 C/C genotype in NO synthase is a significant contributing factor for increasing the risk of essential hypertension.
Hypertension 2002 Apr
PMID:The T-786-->C mutation in endothelial nitric oxide synthase is associated with hypertension. 1196 50

A 55-year-old man with hypertension was scheduled for resection of spinal tumor at S1 in the prone position. Anesthesia was induced with midazolam 10 mg, fentanyl 0.2 mg and vecuronium 10 mg, and maintained with sevoflurane 1.5-2% in oxygen 3 l x min(-1) and fentanyl 0.4 mg. When the interspinal ligament was handled, severe ST depression on the ECG was observed for 1 minute, followed by ventricular tachycardia (VT). Immediately, 60 mg of lidocaine was administered intravenously, and ventricular rhythm recovered to sinus rhythm with normal ST level within a few minutes, but the surgery was postponed. In the preoperative examinations, the patient had been evaluated as a low risk case except for a long history of hypertension. Coronary spasm was suspected to have induced VT, because it followed severe ST depression. This experience taught us that in order to avoid critical arrhythmia, patients under general anesthesia, especially those undergoing surgery in the prone position, require particular attention because of the difficulty in cardiac resuscitation.
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PMID:[Case of ventricular tachycardia induced by coronary spasm during surgery in prone position]. 1550 Jan 14

Resistance arteries are able to adapt to physiological and pathophysiological stimuli to maintain adequate perfusion according to the metabolic demand of the tissue. Although vasomotor control allows rapid adaptation of lumen diameter, vascular remodeling constitutes an active process that occurs in response to long-term alterations of hemodynamic parameters. Unfortunately, this initially adaptive process contributes to the pathology of vascular diseases. Recent studies have demonstrated the participation of Rho protein signaling pathways in several cardiovascular pathologies including hypertension, coronary artery spasm, effort angina, atherosclerosis, and restenosis. Functional analyses have further revealed that RhoA-dependent pathways are involved in excessive contraction, migration, and proliferation associated with arterial diseases. The present review focuses on the role of Rho proteins, in particular RhoA, in vascular smooth muscle cells and the involvement of Rho-dependent signaling pathways in resistance artery remodeling, more particularly in relation to hypertension.
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PMID:RhoA and resistance artery remodeling. 1570 42

Angina in the setting of a normal angiogram (NOCAD) occurs in 20-30% of patients undergoing coronary angiography. The etiologies of NOCAD can be anatomically classified into three groups: epicardial disease, coronary microvascular dysfunction, and noncoronary disease. Epicardial disease resulting in NOCAD includes endothelial dysfunction, coronary artery spasm, and coronary artery bridging. Microvascular dysfunction may be secondary to hypertension, cardiomyopathy, infiltrative disease, valvular disease, or idiopathic. Noncoronary artery disease states involving other organs systems such as the pulmonary, gastrointestinal, or musculoskeletal systems can also result in NOCAD. This review focuses on the coronary etiologies of NOCAD. The pathophysiology of disease is discussed as well as a systematic diagnostic strategy. Potential therapeutic options and prognosis are also reviewed.
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PMID:Angina pectoris with a normal coronary angiogram. 1575 52

Rho is a GTPase known to be a major mediator in the formation of stress fibers and focal adhesions, cell morphology, and smooth muscle contraction. Its role in smooth muscle contraction has led to exploration into the connection between Rho-mediated kinase activity and cardiovascular disease. The role of Rho-kinase in calcium sensitization for vascular smooth muscle contraction has recently been characterized. Inappropriate coronary artery vasoconstriction resulting from increased Rho-kinase in the vascular system is likely involved in the pathogenesis of exercise-induced myocardial ischemia, spontaneous coronary artery spasm, and hypertension. In clinical trials, Rho-kinase inhibitors such as fasudil and Y-27632 have demonstrated antiischemic, antivasospastic, and antihypertensive effects. These compounds have also exhibited the ability to blunt progression of cardiomyocyte hypertrophy and cardiac remodeling in heart failure. As such, Rho-kinase inhibition represents a potential novel therapeutic approach in cardiovascular disease.
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PMID:Rho-kinase inhibition in the therapy of cardiovascular disease. 1623 Aug 85

Both hypertension and coronary artery spasm (CAS) are associated with endothelial dysfunction. Thus, a higher incidence of CAS is expected in hypertensive patients. We evaluated the impact of hypertension on CAS with intracoronary acetylcholine (ACh) provocation test. A total of 986 patients (685 hypertensive patients vs 301 normotensive patients) who underwent coronary angiography with ACh provocation test were enrolled. ACh was injected into the left coronary artery in incremental doses of 20, 50 and 100 microg min(-1). Significant CAS was defined as a transient >70% luminal narrowing with concurrent chest pain and/or ST-segment changes. Although the incidences of significant ACh-induced CAS were similar between hypertensive and normotensive patients (35.8 vs 39.2%, P=0.303), multivariate logistic analysis showed that hypertension was negatively associated with ACh-induced CAS (odds ratio: 0.70, 95% confidence interval: 0.51-0.94, P=0.020). The angiographic characteristics of ACh-induced CAS were similar between these two groups. Subgroup analysis regarding the impact of the status of blood pressure control on CAS showed that hypertensive patients with controlled blood pressure had a significantly higher incidence of CAS than those with uncontrolled blood pressure (45.2 vs 27.9%, P<0.001), and that uncontrolled blood pressure was negatively associated with ACh-induced CAS (odds ratio: 0.56, 95% confidence interval: 0.40-0.79, P=0.001). In conclusion, despite the expected endothelial dysfunction, hypertension and uncontrolled blood pressure are negatively associated with CAS, suggesting that the mechanisms and risk factors of CAS may be significantly different from those of coronary artery disease.
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PMID:Impact of hypertension on coronary artery spasm as assessed with intracoronary acetylcholine provocation test. 1945 25

Coronary artery spasm (CAS) is a dangerous complication during cardiac surgery, causing arduous weaning of extracorporeal circulation (ECC) and myocardial tissue loss with consequent left and right ventricular dysfunctions. We describe the case of a 67-year-old man with hypertension and smoking habit, with ECG evidence of lateral myocardial ischemia without symptoms. On this basis, he was investigated with scintigraphy, which confirmed an anterior-lateral area of reversible ischemia and, subsequently, with angiography, which revealed just mild lesion (50%) of diagonal ramus associated with ascending aorta aneurysm: no sign of CAS was detected. Left ventricular function was normal, with mild hypokinesia of the apical segments and trivial aortic regurgitation. The patient underwent ascending aorta replacement with arduous ECC weaning due to CAS: exclusively, the use of intravenous administration of diltiazem led to the solution of this complication. Even if medical therapy is generally efficacious for this complication, the diagnosis is very complicated when it appears in the operating room immediately after cardiac surgery because of the lack of any useful device. The difficulty of diagnosis in the operating room might compromise patient outcome. In our opinion, when ECC weaning is complicated by several episodes of malignant tachyarrhythmia and there is the suspicion of underlying ischemic cause without other obvious causes, CAS must be considered and empirical therapy with calcium channel blockers should be used.
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PMID:Recurrent ventricular fibrillation due to coronary artery spasm immediately after ascending aorta replacement. 1947 58


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