Home About us Contact
|
Home About us Contact | ||
|
|
||
Acute Myocardial Ischemia (acute + myocardial_ischemia)
Selected AbstractsNuclear Cardiology in the Evaluation of Acute Chest Pain in the Emergency DepartmentECHOCARDIOGRAPHY, Issue 6 2000Brian G. Abbott M.D. Only a minority of patients presenting to the emergency department (ED) with acute chest pain will eventually be diagnosed with an acute coronary syndrome. The majority will have an electrocardiogram that is normal or nondiagnostic for acute myocardial ischemia or infarction. Typically, these patients are admitted to exclude myocardial infarction despite a very low incidence of coronary artery disease. However, missed myocardial infarctions in patients who are inadvertently sent home from the ED have significant adverse outcomes and associated legal consequences. This leads to a liberal policy to admit patients with chest pain, presenting a substantial burden in terms of cost and resources. Many centers have developed chest pain centers, using a wide range of diagnostic modalities to deal with this dilemma. We discuss the methods currently available to exclude myocardial ischemia and infarction in the ED, focusing on the use of myocardial perfusion imaging as both an adjunct and an alternative to routine testing. We review the available literature centering on the ED evaluation of acute chest pain and then propose an algorithm for the practical use of nuclear cardiology in this setting. [source] Regulation and Role of the Presynaptic and Myocardial Na+/H+ Exchanger NHE1: Effects on the Sympathetic Nervous System in Heart FailureCARDIOVASCULAR THERAPEUTICS, Issue 2 2007Kirsten Leineweber ABSTRACT In acute myocardial ischemia and in chronic heart failure, sympathetic activation with excessive norepinephrine (NE) release from and reduced NE reuptake into sympathetic nerve endings is a prominent cause of arrhythmias and cardiac dysfunction. The Na+/H+ exchanger NHE1 is the predominant isoform in the heart. It contributes to cellular acid,base balance, and electrolyte, and volume homeostasis, and is activated in response to intracellular acidosis and/or activation of guanine nucleotide binding (G) protein-coupled receptors. NHE1 mediates its signaling via protein kinases A (PKA) or C (PKC). In cardiomyocytes, NHE1 is restricted to specialized membrane domains, where it regulates the activity of pH-sensitive proteins and modulates the driving force of the Na+/Ca2+ exchanger. During acute ischemia/reperfusion and in heart failure the activity/amount of NHE1 is increased, leading to intracellular Ca2+ overload and promoting structural (apoptosis, hypertrophy) and functional (arrhythmias, hypercontraction) myocardial damage. In sympathetic nerve endings, increased NHE1 activity results in the accumulation of axoplasmic Na+ that diminishes the inward and/or favors the outward transport of NE via the neuronal norepinephrine transporter (NET). The increased NE levels within the nerve,muscle junction facilitate the sustained stimulation of myocardial ,- and ,-adrenoceptors (ARs), which in turn aggravate the increases in myocardial NHE1 activity and the associated deleterious effects. Furthermore, the responsiveness of the ,-AR declines overtime, which results in further release of NE, initiating a vicious cycle. Accordingly, NHE1 is a potential candidate for targeted intervention to suppress this feedback loop. [source] Cardiac troponins T and I in patients with end-stage renal disease: The relation with left ventricular mass and their prognostic valueCLINICAL CARDIOLOGY, Issue 12 2004Adnan Abaci M.D. FESC Abstract Background:Cardiac troponins are frequently elevated in patients with end-stage renal disease (ESRD) in the absence of acute myocardial ischemia. The cause and prognostic value of cardiac troponin elevations in such patients are controversial. Hypothesis:The aims of this study were (1) to define the incidence of cTnT and cTnI elevations in patients with ESRD, (2) to evaluate the relationship between troponin elevations and leftventricularmass index (LVMI), and (3) to evaluate the prognostic value of elevations in cTnT and cTnI prospectively. Methods:We included 129 patients with ESRD (71 men, age 44 ± 16 years) with no clinical evidence of coronary artery disease. All patients underwent cardiac examinations, including medical history, physical examination, electrocardiogram, andtransthoracic echocardiography. Left ventricular mass index was calculated and all patients were followed for 2 years. Results:The cTnT concentration was > 0.03,0.1 ng/ml in 27 (20.9%) and > 0.1 ng/ml in 27 (20.9%) of the 129 patients. The cTnI concentration was > 0.5 ng/ml in 31 (24%) of 129 patients. Multiple logistic regression analysis identified LVMI (p < 0.001), diabetes (p = 0.001), and serum albumin level (p= 0.009) as a significant independent predictor for elevated cTnT. Left ventricular mass index was the only significant independent predictor for elevated cTnI (p = 0.002). There were 25 (19.4%) deaths during follow-up. Multivariable analysis showed that elevation of cTnT and cTnI did not emerge as an independent predictor for death. Serum albumin level (p < 0.001) was the strongest predictor of mortality, followed by age (p = 0.002) and LVMI (p = 0.005). Conclusions:Cardiac troponin T and I related significantly to the LVMI. The increased serum concentration of cardiac troponins probably originates from the heart; however, they are not independent predictors for prognosis. [source] Spontaneous coronary artery dissectionCLINICAL CARDIOLOGY, Issue 7 2004Francis Q. Almeda M.D. Abstract Spontaneous coronary artery dissection (SCAD) is an unusual cause of acute myocardial ischemia with complex pathophysiology. This paper reviews the major diagnostic and therapeutic issues of this rare but important disease. The diagnosis of SCAD should be strongly considered in any patient who presents with symptoms suggestive of acute myocardial ischemia, particularly in young subjects without traditional risk factors for coronary artery disease (especially in young women during the peripartum period or in association with oral contraceptive use). Urgent coronary angiography is indicated to establish the diagnosis and to determine the appropriate therapeutic approach. The decision to pursue medical management, percutaneous coronary intervention, or surgical revascularization is based primarily on the clinical presentation, extent of dissection, and amount of ischemic myocardium at risk. [source] Postoperative troponin I values: Insult or injury?CLINICAL CARDIOLOGY, Issue 10 2000Keith A. Horvath M.D. Abstract Background: Troponin I (TnI) is increasingly employed as a highly specific marker of acute myocardial ischemia. The value of this marker after cardiac surgery is unclear. Hypothesis: The purpose of this study was to measure serum TnI levels prospectively at 1, 6, and 72 h after elective cardiac operations. In addition, TnI levels were measured from the shed mediastinal blood at 1 and 6 h postoperatively. Serum values were correlated with cross clamp time, type of operation, incidence of perioperative myocardial infarction, as assessed by postoperative electrocardiograms (ECG) and regional wall motion, as documented by intraoperative transesophageal echocardiography (TEE). Methods: Sixty patients underwent the following types of surgery: coronary artery bypass graft (CABG) (n = 45), valve repair/replacement (n = 10), and combination valve and coronary surgery (n = 5). Myocardial protection consisted of moderate systemic hypothermia (30,32°C), cold blood cardioplegia, and topical cooling for all patients. Results: Of 60 patients, 57 (95%) had elevated TnI levels, consistent with myocardial injury, 1 h postoperatively. This incidence increased to 98% (59/60) at 6 h postoperatively. There was a positive correlation between the length of cross clamp time and initial postoperative serum TnI (r = 0.70). There was no difference in the serum TnI values whether or not surgery was for ischemic heart disease (CABG or CABG + valve versus valve). There were no postoperative myocardial infarctions as assessed by serial ECGs. There was no evidence of diminished regional wall motion by TEE. Levels of TnI in the mediastinal shed blood were greater than assay in 58% (35/60) of the patients at 1 h and in 88% (53/60) at 6 h postoperatively. Patients who received an auto-transfusion of mediastinal shed blood (n = 22) had on average a 10-fold postoperative increase in serum TnI levels between 1 and 6 h. Patients who did not receive autotransfusion average less than doubled their TnI levels over the same interval. At 72 h, TnI levels were below the initial postoperative levels but still indicative of myocardial injury. Conclusion: Postoperative TnI levels are elevated after all types of cardiac surgery. There is a strong correlation between intraoperative ischemic time and postoperative TnI level. Further elevation of TnI is significantly enhanced by reinfusion of mediastinal shed blood. Despite these postoperative increases in TnI, there was no evidence of myocardial infarction by ECG or TEE. The postoperative TnI value is even less meaningful after autotransfusion of shed mediastinal blood. [source] | ||||||||||