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

Psychological stress has been shown to trigger angina and myocardial ischemia in patients with coronary artery disease. However, the mechanisms by which stress may trigger cardiac events has yet to be fully elucidated. Twenty five patients underwent radionuclide ventriculography during a multiple stress challenge. Plasma volume was assessed during rest and at the end of the stress task. Flow-mediated dilatation was also measured. Controlling for endothelial function and medications, patients with ischemia had greater reductions in plasma volume than non-ischemic patients. Reduced plasma volume may be one mechanism by which mental stress may increase the risk for acute coronary events.
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PMID:Changes in plasma volume associated with mental stress ischemia in patients with coronary artery disease. 1625 64

Myocardial ischemia provoked in the laboratory during mental stress (MSI) in patients with stable coronary artery disease (CAD) predicts subsequent clinical events. The pathophysiology of MSI differs from that of exercise ischemia, and the mechanisms tying MSI to poor prognosis are not known. C-reactive protein (CRP) is a risk marker for cardiovascular events in patients with CAD, but little is known regarding the relationship of CRP to MSI. The purpose of this study was to examine the association of CRP to risk of MSI in CAD patients. Eighty-three patients with stable CAD underwent simultaneous single-photon emission computed tomography (SPECT) imaging with technetium-99m tetrofosmin myocardial perfusion imaging (MPI) and transthoracic echocardiography (TTE), at rest and during MS induced by laboratory mental stress. Serum CRP levels were measured 24 h after MS. MSI was defined by the presence of a new perfusion defect on SPECT and/or new regional wall motion abnormality on TTE during MS. Of the 83 patients, 30 (36%) developed MSI. There was no difference in gender, sex, BMI, histories of diabetes, hypertension, smoking, lipid profile, medications used (including statins, beta-blockers, ACE inhibitors, and aspirin), or hemodynamic response during MS between those with and without MSI. In univariate logistic regression analysis, each unit (1 mg/L) increase in CRP level was associated with 20% higher risk of MSI (OR 1.2, 95% CI 1.01-1.39, P=.04). This relationship remained in multivariate models. These data suggest that levels of CRP may be a risk marker for MSI in patients with CAD.
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PMID:C-reactive protein and vulnerability to mental stress-induced myocardial ischemia. 1738 Jan 91

Mental and emotional stress can provoke transient ischemia and acute coronary syndrome in vulnerable patients. Furthermore, those patients so provoked are at increased risk for recurrent cardiac events and early death. Viable psychological treatments to improve prognosis exist, and preliminary trials demonstrate their efficacy with regard to short- and long-term outcomes, as well as economic savings. These findings heighten the need for efforts directed toward the complete identification of the differential pathophysiology of mental stress-induced ischemia, with an eye toward development of diagnostic tests and establishment of risk stratification algorithms that can be applied in the clinical setting. Ongoing research in this vein is identifying unique aspects of the brain-heart relationship during mental stress that underlie the cognitive and emotional aspects of mental stress, and the "dow nwind" pathways by which distinct patterns of brain activity during mental stress can provoke otherwise silent myocardial ischemia. This research is making important contributions to the larger clinical goals associated with diagnostic testing, risk stratification, and treatment of patients at risk for mental stress-induced ischemia and poorer prognosis.
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PMID:The heart-brain interaction during emotionally provoked myocardial ischemia: implications of cortical hyperactivation in CAD and gender interactions. 1745 47

Apical ballooning is a novel clinical entity reported in different contexts of physical and psychological stress, which is more common in middle-aged women. Of unknown etiology, the syndrome is characterized by a sudden and transient dilatation of the left ventricular apex in the absence of obstructive atherosclerotic coronary disease or evidence of myocardial necrosis, with total late recovery of ventricular function. The authors report the case of a 53-year-old woman who was admitted to the emergency room with left arm ischemia and low cardiac output, requiring ventilatory support. Left catheterization showed typical medial and apical myocardial dysfunction, with normal coronary arteries. Transesophageal echocardiography revealed a thrombus attached to the lower face of the aortic arch, which probably explained the thromboembolism of the arm but was unlikely to be the cause of the left ventricular dysfunction since there were no enzymatic or electrocardiographic signs of myocardial necrosis and normal wall motion was fully recovered.
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PMID:Stress cardiomyopathy in thromboembolic arterial disease. 1754 84

The term "electrical storm" (ES) indicates a state of cardiac electrical instability manifested by several episodes of ventricular tachyarrhythmias (VTs) within a short time. In patients with an implantable cardioverter defibrillator (ICD), ES is best defined as 3 appropriate VT detections in 24 h, treated by antitachycardia pacing, shock or eventually untreated but sustained in a VT monitoring zone. The number of shocks and inappropriate detections are irrelevant for the definition. ES occurs in approximately 25% of ICD patients within 3 years, with typically 5-55 individual VTs within one storm. Potential triggers can be found in approximately 66% of patients and include new/worsened heart failure, changes in antiarrhythmic medication, context with other illness, psychological stress, diarrhea, and hypokalemia. In most patients, ES consists of monomorphic VT indicating the presence of reentry while ventricular fibrillation indicating acute ischemia is rare. ES seems to have a low immediate mortality (1%) but frequently (50-80%) leads to hospitalization. Long-term prognostic implications of ES are unclear. The key intervention in ES is reduction of the elevated sympathetic tone by beta blockers and frequently benzodiazepines. Amiodarone i.v. has also been successful and azimilide seems promising while class I antiarrhythmic drugs are usually unsuccessful. Substrate mapping and VT ablation may be useful in treatment and prevention of ES. Prevention of ES requires ICD programming systematically avoiding unnecessary shocks (long VT detection, antitachycardia pacing where ever possible) which otherwise can fuel the sympathetic tone and prolong ES.
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PMID:Electrical storm in patients with an implanted defibrillator: a matter of definition. 1797 Sep 63

Physical and mental stressors result in increased inflammation markers in populations free of coronary artery disease (CAD). However, inflammatory responses to mental and exercise challenges have not been established in patients with CAD. This study investigated the responses of inflammatory markers, including C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1, in patients with CAD after successful elective percutaneous coronary intervention (n = 36, 59 +/- 8 years of age, 33% women) and healthy controls without a history of CAD (n = 28, 54 +/- 10 years of age, 36% women). Increases in inflammatory markers were examined in response to mental challenge tasks (anger recall and mental arithmetic) and treadmill exercise. Stress echocardiography was used to rule out stress-induced ischemia as a possible confounding factor. Results showed that CRP increased significantly to mental challenge and exercise (p values <0.01), and CRP responses were higher in patients with CAD than in controls (change in mental arithmetic 0.19 +/- 0.11 vs 0.01 +/- 0.03 mg/L, p = 0.003; change in exercise 0.57 +/- 0.11 vs 0.08 +/- 0.0.03 mg/L, p = 0.001). Increased norepinephrine responses were related to larger CRP and IL-6 increases to mental challenge tasks (p values <0.05). Exercise elicited increased CRP, IL-6, and soluble intercellular adhesion molecule-1 levels (p values <0.01), and these responses were larger than with mental challenge tasks (p values <0.05). In conclusion, mental stress and exercise induce increased levels of inflammatory markers in patients with CAD. These stress-induced increases are larger than in healthy subjects, occur in the absence of myocardial ischemia, and are related to the neurohormonal stress response.
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PMID:Effects of acute mental stress and exercise on inflammatory markers in patients with coronary artery disease and healthy controls. 1832 37

This article reviews what our colleagues have found as to how ischemic injury or cell death develop in myocardium through Ca(2+)-dependent protease calpain and how compensatory responses evolve through activation of intracellular signaling molecules including PKC isoforms, MAP kinase family enzymes and PI3 kinase. We also addressed how restraint or other psychological stress evokes hypertension and cardiovascular responses in signaling molecules or genes. Unexpectedly, carbon monoxide protects heart and cardiogenic cells against ischemia-resperfusion injury. When I think back, the unresolved cases of autopsies provided ideas for experimental study, which then taught us how the other cases died.
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PMID:Pursuing enigmas on ischemic heart disease and sudden cardiac death. 1904 46

Myocardial ischemia that results from emotional provocation occurs in as many as 30% to 50% of patients with coronary artery disease during the discourse of their lives. This emotionally provoked or mental stress ischemia is associated with poor prognosis, with emerging treatment strategies. This article outlines the conceptual constructs that support the pathophysiologic underpinnings, and biobehavioral aspects associated with this mental stress ischemia. We review a biobehavioral model in which cognitive stress is transduced in the brain. The response of the brain to psychosocial stress is a highly sophisticated and integrated process by which sensory inputs are evaluated and appraised for their importance in relation to previous experience and current goals. The biologic consequences of such stress transduced in the central nervous system has its effect on cardiovascular flow and function through changes in autonomic balance, which result in various biologic processes that culminate in the perturbation of flow and function of the heart.
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PMID:Heart-brain interactions in mental stress-induced myocardial ischemia. 1923 29

Left ventricular ballooning syndrome (LVBS), also known as Takotsubo cardiomyopathy, is characterized by regional left ventricular dysfunction associated with severe psychological stress. T2 weighted cardiac magnetic resonance (CMR) can identify myocardial edema due to ischemia or other insults. A standard clinical CMR scan with double inversion recovery fast spin echo T2 weighted sequences was performed on consecutive patients with LVBS. T2 signal was compared in myocardial segments with normal and impaired function based on systolic wall thickening (SWT). Eight LVBS patients were identified, all female, with a median age of 61 years and median left ventricular ejection fraction of 52%. Four patients had apical ballooning and four had mid-wall or basal ballooning. In severely dysfunctional segments (those with SWT < 25%), the median percentage of high T2 signal was 85 compared with 35 in those with SWT > 25% (P < 0.001). When the segments were categorized into tertiles based on SWT, the percentage of high T2 signal was greatest in segments with the worst function (68% vs. 43% vs. 31%, P = 0.005). In the five patients who returned for follow up, there was a significant reduction in high T2 signal compared with baseline in those segments that were initially severely dysfunctional (85% vs. 35%, P < 0.001). In conclusion, we describe elevated T2 signal consistent with myocardial edema in patients with LVBS. The T2 signal is highest in myocardium with the most impaired function and resolves over time.
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PMID:Cardiovascular magnetic resonance T2 signal abnormalities in left ventricular ballooning syndrome. 2017 95

Previous studies of patients with stable coronary artery disease have demonstrated that decreases in the left ventricular ejection fraction (LVEF) during acute mental stress are predictive of adverse clinical outcomes. The aim of the present study was to examine the prospective relation of mental stress on clinical outcomes in a sample of 138 patients with stable coronary artery disease. Patients underwent mental stress testing and were followed for a median of 5.9 years to assess the occurrence of the combined end point of myocardial infarction or all-cause mortality. There were 32 events (17 nonfatal myocardial infarctions and 15 deaths) over the follow-up period. Of the 26 patients who exhibited myocardial ischemia during mental stress testing, 11 (42%) sustained subsequent clinical events, compared to 21 of the 112 patients (19%) who showed no mental stress-induced ischemia. LVEF change during mental stress was also related to the clinical events in a graded, continuous fashion, with each 4% decrease from the LVEF at rest associated with an adjusted hazard ratio of 1.7, (95% confidence interval 1.1 to 2.6, p = 0.011). In conclusion, reductions in the LVEF during mental stress are prospectively associated with adverse clinical outcomes.
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PMID:Prognosis after change in left ventricular ejection fraction during mental stress testing in patients with stable coronary artery disease. 2010 85


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