Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BACKGROUND. Acute closure remains a significant limitation of percutaneous transluminal coronary angioplasty (PTCA) and underlies the majority of ischemic complications. This study details the clinical and angiographic characteristics of a series of patients receiving an intracoronary stent device to manage acute and threatened closure and presents the early clinical results. METHODS AND RESULTS. From October 1989 through June 1991, 115 patients undergoing PTCA received intracoronary stents to treat acute or threatened closure in 119 vessels. Sixty-three percent had multivessel coronary disease, 33 (29%) had undergone prior coronary artery bypass grafting (CABG), and 52 (45%) had had previous PTCA. Using the American College of Cardiology/American Heart Association (ACC/AHA) classification, 15% of lesions were class A, 55% were class B, and 30% were class C. Eight patients were referred with severe coronary dissection and unstable angina after PTCA at other institutions. Acute closure was defined as occlusion of the vessel with TIMI (Thrombolysis in Myocardial Infarction) 0 or 1 flow immediately before stent placement. Threatened closure required two or more of the following criteria: 1) a residual stenosis greater than 50%, 2) TIMI grade 2 flow, 3) angiographic dissection comprising extraluminal dye extravasation and/or a length of greater than 15 mm, 4) evidence of clinical ischemia (either typical angina or ECG changes). Twelve vessels (10%) met the criteria for acute closure, and 87 vessels (73%) satisfied the criteria for threatened closure. Twenty vessels (17%) failed to meet two criteria. Stenting produced optimal angiographic results in 111 vessels (93%), with mean diameter stenosis (+/- 1 SD) reduced from 83 +/- 12% before to 18 +/- 29% after stenting. Overall, in-hospital mortality was 1.7% and CABG was required in 4.2%; Q wave myocardial infarction (MI) occurred in 7% and non-Q wave MI in 9%. Stent thrombosis occurred in nine patients (7.6%). For the 108 patients who presented to the catheterization laboratory without evolving MI, Q wave MI occurred in 4% and non-Q wave MI occurred in 7%. Angiographic follow-up has been performed in 81 eligible patients (76%), and 34 patients (41%) had a lesion of greater than or equal to 50%. CONCLUSIONS. This stent may be a useful adjunct to balloon dilatation in acute or threatened closure. Randomized studies comparing this stent with alternative technologies are required.
 ...
PMID:Intracoronary stenting for acute and threatened closure complicating percutaneous transluminal coronary angioplasty. 153 28

Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. We analyzed 2,304 serial ECGs at study entry (admission), day 2, day 3, and predischarge (mean, 10.2 +/- 2 days) from 576 patients with creatine kinase MB confirmed acute non-Q wave MI to determine what percentage of patients with early ST segment elevation culminated in subsequent Q wave development. Of this group, 187 patients (32%) exhibited 1 mm or greater ST segment elevation in two or more contiguous entry ECG leads. Of those patients whose non-Q wave MI could be localized on the basis of diagnostic admission ST segment shifts, the prevalence of early ST segment elevation was 43% (187 of 439). The sum total mean (+/- SD) peak ST segment elevation by lead group (anterior, inferior, lateral) was 4.0 +/- 2.4, 4.5 +/- 2.4, and 2.5 +/- 0.6 mm, respectively. Despite this, only 20% of patients with ST segment elevation (37 of 187) developed Q waves. Of 252 patients who exhibited early ST segment depression or T wave inversion or both, 39 (15%) evolved subsequent Q waves. Thus, while the prevalence of early ST segment elevation in acute evolving non-Q wave MI was higher than previously reported, 80% of patients with and 85% of patients without ST segment elevation and absent Q waves on the admission ECG did not develop subsequent Q waves during a 2-week period of observation (p = NS). In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.
 ...
PMID:ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction. 264 62

Although Q wave and non-Q wave MI are often referred to as "transmural" and "nontransmural," there is no anatomic evidence to justify this distinction. Nevertheless, a distinction is important, because the two entities have a different prognosis. At the present time, between 25% and 35% of MIs are non-Q wave. They are frequently observed in patients with previous coronary events. They occur in a relatively older population and involve a slightly higher proportion of women than do Q wave MIs. The degree of cardiac damage is less, reflected by a smaller rise in enzyme level and less impairment of left ventricular ejection fraction; early reperfusion may occur, after spontaneous thrombolysis or resolution of coronary spasm. The immediate mortality rate is half that of Q wave MI but identical in the long term. Reinfarction and angina are more frequent because of a peri-infarction zone of ischemia maintained by a high-grade coronary stenosis and inadequate collateral circulation. Early characterization of those MIs likely to progress is important. Diltiazem seems effective in this context if given between 24 and 72 hours of the onset of the event. Other therapeutic approaches need further assessment.
 ...
PMID:"Non-Q wave," alias "nontransmural," myocardial infarction: a specific entity. 264 80

Early ischemia, defined as angina with transient ST-T changes during hospitalization, 24 hr or more after an acute myocardial infarction (MI), was observed in 79 (18%) of a consecutive series of 449 patients surviving an MI and catheterized a mean of 10 +/- 3 days after admission. Three clinical factors present 24 hr after admission could identify patients at low, medium, and high risk of factors had a risk greater than 50% and the 118 patients with Q wave MI, no previous angina, and absence of risk factors had a risk of less than 8%. The angiographic correlates of early ischemia were number of vessels with 70% or more stenosis (2.1 +/- 0.8 vs 1.7 +/- 0.8/patient, p less than .0001), number of diseased coronary artery segments (2.8 +/- 1.4 vs 2.1 +/- 1.2, p less than .0001), left anterior descending coronary involvement (77% vs 62% of patients, p = .01), number of normally contractile segments at jeopardy because of a coronary stenosis (1.9 +/- 1.3 vs 1.3 +/- 1.1/patient, p less than .0002), collateral circulation at jeopardy (24% vs 15% of patients, p less than .005), and fewer collateral vessels distal to a tight stenosis (59 vs 72% of patients, p = .04). The stepwise logistic regression retained one angiographic and two clinical independent predictors of early ischemia: number of diseased vessels (p = .0008), presence of a non-Q wave MI (p = .0027), and previous angina (p = .017).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Early postinfarction ischemia: clinical, angiographic, and prognostic significance. 356 14

In the 10 years since our previous review of this topic, the acute coronary syndromes (Q wave myocardial infarction [QMI], non-Q wave MI [NQMI], and unstable angina) have been more clearly categorized. Many of the differences delineated between QMI and NQMI still hold: a less extensive infarction and a lower in-hospital mortality, but a larger degree of jeopardized myocardium leading to a higher incidence of reinfarction and recurrent angina. The pathophysiology of NQMI appears to be similar to that of unstable angina except for the greater incidence and extent of thrombus formation and coronary artery occlusion with NQMI. Prognostic studies have shown that ST depression and anterior infarct location are associated with a greater risk for posthospital clinical events than the findings of ST elevation and other infarct locations. Symptom-limited stress testing using electrocardiogram and thallium-201 imaging are now recommended before discharge or in the early postdischarge period, with coronary arteriography recommended for evidence of residual ischemia. Aspirin and low dose heparin should be administered on admission after NQMI to decrease further thrombus formation, and aspirin continued in the posthospital period. Diltiazem administration is recommended in NQMI without evidence of pulmonary congestion to prevent recurrent nonfatal acute myocardial infarction. Percutaneous transluminal coronary angioplasty and surgical revascularization should be reserved for patients with NQMI with residual ischemia.
 ...
PMID:The non-Q wave myocardial infarction revisited: 10 years later. 912 24

The role of antithrombotic therapy has been studied in patients with acute coronary ischemia without ST segment elevation. Unfractionated heparin (UFH) has been found to decrease the rate of myocardial infarction (MI), and to reduce overall mortality and recurrent MI in a series of trials in patients with unstable angina and non-Q wave MI. UFH is limited due to its unpredictable antithrombotic effect, poor bioavailability when given subcutaneously, requirement for hospitalization and need for frequent laboratory monitoring. Conversely, low molecular weight heparins (LMWHS) offer a number of advantages over UFH. LMWHs have a predictable antithrombotic response, good bioavailability following subcutaneous administration and longer half-life than UFH, require less frequent monitoring than UFH and can be administered in fixed or weight-adjusted subcutaneous dosages once or twice daily. The safety and efficacy of the LMWH enoxaparin are evaluated in the Thrombolysis in Myocardial Infarction (TIMI) 11 program. TIMI 11 A was designed to compare the safety and tolerability of two dosage regimens of enoxaparin in patients with unstable angina or non-Q wave MI, whereas TIMI 11B was designed as a phase III trial, comparing the efficacy and safety of enoxaparin with those of UFH in the acute phase, and the efficacy and safety of extended administration of LMWH with those of placebo for 45 days. TIMI 11A found that the rate of major hemorrhage was significantly lower for the lower enoxaparin dose (1.0 mg/kg). The results of the published studies indicate that LMWHs are effective in reducing major ischemic outcomes in patients with unstable angina and non-Q wave MI. The results of the TIMI 11B trial will be available in late 1998.
 ...
PMID:Management of acute coronary syndromes with low molecular weight heparin: TIMI 11A and 11B. 977 29

The aim of our study was to evaluate whether a single dose of cerivastatin at the time of admission of patients with unstable angina pectoris (UAP) or non-Q-wave myocardial infarction (NQMI) can influence the serum level of C-reactive protein (CRP), interleukin-6 (IL-6) and interleukin-8 (IL-8) 24 h later. Forty-four patients with rest chest pain and subendocardial ischemia on ECG were randomized to receive cerivastatin 0.3 mg at the time of admission (group C+) to standard therapy or to remain just on standard therapy (group C-). Blood samples for determination of troponin I (TI), CRP, IL-6 and IL-8 were collected at admission (entry level) and 24 h later (final level). Patients with non-physiological baseline levels of TI, as well as patients with progression to Q wave MI were excluded. All baseline, clinical and demographic data and final values of TI were comparable in the two groups. In patients treated with cerivastatin (group C+, n = 13) we observed decrease in the CRP level (-6.73 +/- 3.93 mg/L); on the other hand, in group C- (n = 17) the CRP level increased (+7.92 +/- 2.77 mg/L, p = 0.004). Similar differences were observed also in IL-6: in group C+ the level was significantly reduced as compared with the increase in group C- (-0.76 +/- 0.52 vs. 4.58 +/- 1.49 ng/L, p = 0.005). The level of IL-8 was not affected. Our results suggest that early treatment with cerivastatin can decrease the serum level of CRP and IL-6 in patients with UAP/NQMI; this might positively influence their prognosis. Nevertheless, further studies are needed to support this hypothesis.
 ...
PMID:The effect of early treatment by cerivastatin on the serum level of C-reactive protein, interleukin-6, and interleukin-8 in the patients with unstable angina and non-Q-wave myocardial infarction. 1284 42

Cangrelor is a new parenteral adenosine diphosphate P2Y12 receptor inhibitor with rapid, profound and reversible inhibition of platelet activity. The aim of this meta-analysis was to evaluate efficacy and safety of this new agent in patients undergoing percutaneous coronary intervention (PCI). We searched PubMed, Cochrane Library, EMBASE, Web of Science and CINAHL databases from the inception through April 2013. Randomized controlled trials (RCTs) comparing cangrelor with control (clopidogrel/placebo) were selected. We used the random-effects models to calculate the risk ratio. The primary efficacy outcome was risk of myocardial infarction, and the primary safety outcome was TIMI major bleeding at 48 h. Three RCTs included a total of 25,107 participants. Effects of Cangrelor were not different against comparators for myocardial infarction (MI) (Risk ratio [RR] 0.94, 95% confidence interval [CI] 0.78-1.13) and all-cause mortality (RR 0.72, 95% CI 0.36-1.43). However, cangrelor significantly reduced the risk of ischemia-driven revascularization (RR 0.72, 95% CI 0.52-0.98), stent thrombosis (RR 0.60, 95% CI 0.44-0.82) and Q wave MI (RR 0.53, 95% CI 0.30-0.92) without causing extra major bleeding (Thrombolysis in Myocardial infarction criteria) and severe or life-threatening bleeding (Global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries criteria). Separate analysis against only clopidogrel also showed similar findings except Q wave MI outcome. Use of cangrelor during PCI might reduce the risk of ischemia-driven revascularization and stent thrombosis, without causing extra major bleeding.
 ...
PMID:Cangrelor for patients undergoing percutaneous coronary intervention: evidence from a meta-analysis of randomized trials. 2405 5

This study aimed to investigate the efficacy of calcitriol on Ischemia-reperfusion Injury (IRI) and inflammatory biomarkers in patients with non-ST-segment elevation acute coronary syndromes (NSTEACS) undergoing elective Percutaneous Coronary Intervention (PCI). A total of 72 patients with NSTEACS were randomly divided into two groups: (1) the calcitriol-treated group, treated with three mcg intravenous calcitriol administered before PCI (n = 36) and (2) the control-treated group (n = 36) The serum high-sensitivity C-reactive protein (hs-CRP), high-sensitivity interleukin-6 (hs-IL-6), creatinine kinase (CK)-MB and cardiac troponin I (cTnI) levels were measured before PCI and 24 h after PCI in both groups. The patients were followed up for the detection of the prevalence of major adverse cardiac events (MACE) in 180 days after PCI in both groups. Compared to pre-PCI, the serum hs-CRP, hs-IL-6, CK-MB, and cTnI levels were increased at 24 h after PCI (all p < 0.05) in both groups. However, change in the levels of hs-CRP and hs-IL-6 were significant (p = 0.04 and p = 0.02, respectively). Changes in the levels of CK-MB and cTnI were non-significant (p = 0.15 and p = 0.39, respectively). No MACE (death, Q wave MI, target vessel revascularization, ischemic stroke) was detected in any patient in any group during a 3-month follow-up. Administration of calcitriol in patients with non-ST-segment elevation acute coronary syndromes undergoing elective PCI can attenuate the increase in serum inflammatory biomarkers in the serum (hs-CRP and hs-IL-6) and thus decrease the inflammatory reaction caused by PCI.
 ...
PMID:The Potential Effect of Intravenous Calcitriol on the Ischemia-Reperfusion Process and Inflammatory Biomarkers in Patients Following Percutaneous Coronary Intervention (PCI). 3280 7