Antineoplastic Agents ; adverse effects ; therapeutic use ; Diarrhea ; chemically induced ; Drug Delivery Systems ; methods ; Exanthema ; chemically induced ; Humans ; Leukopenia ; chemically induced ; Lung Diseases, Interstitial ; chemically induced ; Myocardial Infarction ; chemically induced ; Neoplasms ; drug therapy ; Tumor Lysis Syndrome ; etiology

Objective The benefit of short-term dual antiplatelet therapy (DAPT) following second-generation drug-eluting stents implantation has not been systematically evaluated. To bridge the knowledge gap, we did a meta-analysis to assess the efficacy of ≤6 months versus ≥12 months DAPT among patients with second-generation drug-eluting stents.Methods We searched online databases and identified randomized controlled trials that assess the clinical impact of short-term DAPT (≤6 months) published before March 3, 2016. The efficacy endpoints included the incidence of all-cause death, myocardial infarction, cerebrovascular accidents, and definite or probable stent thrombosis. Safety endpoint defined as major bleeding was also evaluated and discussed.Results We included 5 trials that randomized 9473 participants (49.8%, short-term DAPT duration vs. 50.2%, standard duration). A total of 9445 (99.7%) patients reported the efficacy endpoints, and the safety endpoint was available from 4 studies (n=8457). There was no significant difference in efficacy endpoints between short-term and standard DAPT duration (≥12 months) [risk ratio (RR) 0.96; 95% confidence intervals (CI), 0.80-1.15]. Short-term DAPT duration did not significantly increase the individual risk of all-cause death, myocardial infarction, cerebrovascular accidents, or definite or probable stent thrombosis. Although short-term DAPT obviously reduced risk of major bleeding compared with standard DAPT (RR 0.53; 95% CI, 0.29-0.96), significant publication bias was found when accessing the safety endpoint of the 4 studies (Egger's test, P=0.009).Conclusions The efficacy of short-term DAPT was comparable with that of standard duration DAPT. DAPT less than 6 months may be appropriate for patients receiving second-generation drug-eluting stents implantation.
Drug-Eluting Stents ; Humans ; Myocardial Infarction ; chemically induced ; Platelet Aggregation Inhibitors ; adverse effects ; therapeutic use ; Randomized Controlled Trials as Topic ; Stroke ; chemically induced ; Thrombosis ; chemically induced ; Time Factors

A 49-year-old woman presented with stupor and paraplegia following an induced hypotension. The temporal relationship to the induced hypotension and the absence of a clear embolic source on diagnostic tests support a causal association between the hypotensive episode and the ischemic infarct. However, despite the association, a cause-and-effect relationship could not be automatically inferred.
Brain Infarction/*chemically induced ; Cerebrovascular Accident/*chemically induced ; Female ; Human ; Infarction/*chemically induced ; Middle Aged ; Preoperative Care/*adverse effects ; Propanolamines/*adverse effects ; Spinal Cord/*blood supply ; Spinal Stenosis/surgery

Acute Disease ; Electrocardiography ; Humans ; Myocardial Infarction ; chemically induced ; physiopathology ; Poisoning ; complications ; physiopathology

Cases of acute myocardial infarction (AMI) that occur during pregnancy or postpartum are rarely reported. Ergot derivatives are known to induce the spasmodic contraction of coronary arteries. Administration of ergot derivatives can cause AMI, even in normal healthy people. In several reported cases, ergot derivatives triggered severe AMI during the postpartum period. Here, we report the case of a forty-year-old woman who was successfully impregnated by artificial fertilization and died after treatment with ergot derivatives. The autopsy revealed AMI with severe coronary atherosclerosis. This is the first case that reports aggravation of pre-existent severe coronary atherosclerosis after postpartum infusion of ergot derivtives.
Pregnancy ; *Postpartum Period ; Myocardial Infarction/*chemically induced/diagnosis/pathology ; Maternal Age ; Humans ; Female ; Ergot Alkaloids/*adverse effects ; Coronary Arteriosclerosis/chemically induced/diagnosis/pathology ; Adult

Capecitabine is an orally available chemotherapeutic agent that is converted to 5-fluorouracil (5-FU) after absorbtion. Capecitabine and its active metabolite, 5-FU, have cardiotoxic effects with reported instances of acute coronary syndromes caused due to coronary vasospasm. However, these agents exert toxic effects on cardiovascular system and beyond vasospasm provacation. We report a 46-year-old patient diagnosed as acute inferior infarction who is treated with capecitabine for 3 months due to metastatic breast carcinoma, in whom thrombotic coronary occlusion was observed in angiography. This case demonstrates that apart from vasospasm, coronary thrombosis could be observed after capecitabine treatment, with a possible direct effect of this drug.
Capecitabine ; Coronary Thrombosis ; chemically induced ; Coronary Vasospasm ; chemically induced ; Deoxycytidine ; adverse effects ; analogs & derivatives ; therapeutic use ; Female ; Fluorouracil ; adverse effects ; analogs & derivatives ; therapeutic use ; Humans ; Middle Aged ; Myocardial Infarction ; chemically induced

Bupivacaine is widely used as a local anesthetic. Central nervous system (CNS) and cardiovascular toxicity are well known side effects. However, there has been no report of bupivacaine-induced myocardial injury. We present a case of bupivacaine cardiac toxicity mimicking an acute non-ST segment elevation myocardial infarction, which was eventually diagnosed as bupivacaine-induced cardiac toxicity without CNS toxicity. As soon as a healthy young woman at a private clinic was given a spinal anesthesia of 6mg bupivacaine for hemorrhoidectomy, she developed arrhythmia and hypotension. She was transferred to our emergency room. There was an accelerated idioventricular rhythm with ST segment depression on electrocardiogram, coarse breathing sounds with rales on whole lung field and a butterfly sign on the chest radiograph. 2D transthoracic echocardiography (TTE) revealed reduced left ventricle systolic ejection fraction (approximately 27%). There was regional wall motion abnormality of the left ventricle on 2D TTE and the cardiac marker was increased. We diagnosed the patient as having acute non-ST segment elevation myocardial infarction but her impaired cardiac function improved gradually. On the seventh day from admission, there was a complete spontaneous recovery of cardiac function, and coronary angiography revealed a normal coronary artery. Therefore, we firmly believe that bupivacaine directly injures the cardiac cell.
Myocardium/*pathology ; Myocardial Infarction/chemically induced/*diagnosis/etiology ; Humans ; Heart/*drug effects ; Female ; Electrocardiography ; Diagnosis, Differential ; Bupivacaine/*adverse effects ; Adult

Acute Disease ; Anaphylaxis ; drug therapy ; Epinephrine ; administration & dosage ; adverse effects ; therapeutic use ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; diagnosis ; etiology ; Thrombosis ; chemically induced ; complications

OBJECTIVEA new rat model of cerebral infarction was developed to elucidate the contribution of vascular endothelial cell during focal cerebral infarction formation.

METHODSForty-eight Sprague-Dawley (SD) rats were randomly divided into the model group, sham operation group, and control group for indexes observation of triphenyltetrazolium chloride (TTC) dyeing, neurological deficit, plasma tissue-type plasminogen activator (tPA) activity, plasminogen activator inhibitor (PAI) activity, thromboxane B(2) (TXB(2)) content, and 6-keto-prostaglandin (6-keto-PGF(1alpha)) content.

RESULTS(1) The highest neurological score appeared at 6 h after operation, descending significantly at sequential time. (2) Using TTC dyeing and optical microscope technique, pathological changes in brains were observed. (3) Compared with control group and sham operation groups, there was a decrease in tPA activity of model rats at the initial 12 h after injection of sodium laurate (P < 0.05), PAI activity decreased markedly in the model group at 24 h after injection of sodium laurate. (4) In plasma TXB(2) concentration reached the highest level compared at 6 h after injection of sodium laurate, but there were not obvious differences in plasma 6-keto-PGF(1alpha) concentration among all groups (P > 0.05).

CONCLUSIONFocal cerebral infarction in rats could be induced by some sodium laurate, showing ischemic cerebrum necrosis, function disorder of vascular endothelium-platelet, fibrinolysis abnormality. This model could play an important role in researching the contribution of vascular endothelial cell during cerebral infarction development, preventing and curing by traditional Chinese medicine.

Animals ; Carotid Arteries ; Cerebral Infarction ; chemically induced ; pathology ; physiopathology ; Disease Models, Animal ; Endothelial Cells ; pathology ; Lauric Acids ; administration & dosage ; Ligation ; Rats ; Rats, Sprague-Dawley

Multi-target anticancer drugs have a more comprehensive and extensive range of action,and there is an uncertain risk in the combination of two drugs.A case of acute toxicity induced by erlotinib combined with cabozantinib is reported in this article.
Anilides ; adverse effects ; Drug Eruptions ; etiology ; Drug Therapy, Combination ; adverse effects ; Erlotinib Hydrochloride ; adverse effects ; Humans ; Myocardial Infarction ; chemically induced ; Pyridines ; adverse effects