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Hiroaki Shimokawa - One of the best experts on this subject based on the ideXlab platform.
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1El Research Advances Series Endothelium-Derived Relaxing Factor and Coronary Vasospasm
2016Co-Authors: Paul M. Vanhoutte, Hiroaki ShimokawaAbstract:T he vascular endothelium is the monolayer of squamous cells in direct contact with the circulating blood. Since the first report in 1980 by Furchgott and Zawadzkil of the endothelium-dependency of the relaxation to acetylcholine in isolated arteries, an overwhelming number of find-ings have indicated that this most intimal layer of cells importantly modulates the degree of contrac-tion of the underlying vascular smooth muscle.2-4 It does so by liberating vasoactive substances, such as prostacyclin, a nonprostanoid endothelium-derived relaxing factor (EDRF),2 a hyperpolarizing sub-stance (endothelium-derived hyperpolarizing fac-tor, EDHF),5 and two constrictor substances (endothelium-derived contracting factors, EDCFs)6 (Figure 1). More and more data are emerging sug-gesting that alterations in endothelium-dependent responsiveness of vascular smooth muscle are involved in the pathogenesis of several cardiovas-cular diseases (see Vanhoutte7'8 for reviews). Coronary Vasospasm plays an important pathoge-netic role, not only in variant angina but also in a wide spectrum of ischemic heart disease.9,10 Because Coronary Vasospasm can be provoked by several stimuli with different mechanisms of action that do not induce a pathologic response in normal subjects,11"2 a local nonspecific hypersensitivity of the Coronary artery appears to be involved. This interpretation is in agreement with the clinical obser-vations that Coronary Vasospasm almost invariably occurs at atherosclerotic portions, although the extent of the Coronary artery narrowing varies widely. Among the possible vascular components contributing to the spasm,13 the endothelium may play an important role. This brief review describes the current status of experimental and clinical stud-ies concerning the possible role of EDRFs under normal conditions and in the pathogenesis of coro-nary Vasospasm
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importance of dual induction tests for Coronary Vasospasm and ventricular fibrillation in patients surviving out of hospital cardiac arrest
Circulation, 2009Co-Authors: Yusuke Takagi, Satoshi Yasuda, Jun Takahashi, Morihiko Takeda, Masaharu Nakayama, Kenta Ito, Masanori Hirose, Yuji Wakayama, Koji Fukuda, Hiroaki ShimokawaAbstract:Background: The pathogenesis of out-of-hospital cardiac arrest (OHCA) without organic heart disease has not been fully investigated. Methods and Results: Induction tests were performed in 12 consecutive patients with OHCA for both Coronary Vasospasm with intraCoronary acetylcholine and ventricular fibrillation (VF) with programmed stimulation at 1 month after the event. All patients were positive for 1 of the tests: Coronary Vasospasm alone in 3, VF alone in 2, and both in 7. All patients underwent implantable cardioverter defibrillator (ICD) implantation and appropriate ICD shock was documented in 1 patient. Conclusions: OHCA has a heterogeneous pathogenesis and so dual induction tests are necessary. (Circ J 2009; 73: 767 - 769)
Wenjin Cherng - One of the best experts on this subject based on the ideXlab platform.
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Coronary Vasospasm induced acute Coronary syndrome complicated by life threatening cardiac arrhythmias in patients without hemodynamically significant Coronary artery disease
International Journal of Cardiology, 2007Co-Authors: Mingjui Hung, Chi Wen Cheng, Ning I Yang, Ming Yow Hung, Wenjin CherngAbstract:Abstract Background Coronary Vasospasm-induced electrical and mechanical complications in patients with acute Coronary syndrome and no hemodynamically significant Coronary artery disease are rarely reported. Methods A total of 733 consecutive patients with acute Coronary syndrome admitted to our hospital who subsequently underwent Coronary angiography at our institution were enrolled. Patients who had documented complete atrioventricular block or ventricular fibrillation, no evidence of hemodynamically significant Coronary artery disease on Coronary angiogram, and no other (non-Coronary) cardiac abnormalities were included. Patients were followed for subsequent cardiac events and mortality. Results Over a 6-year period at our institution, acute Coronary syndrome complicated by life-threatening cardiac arrhythmias developed in six patients who had no hemodynamically significant Coronary artery disease with corresponding intra-Coronary ergonovine provocative Coronary Vasospasm. Acute myocardial infarction was diagnosed in five of these patients and variant angina pectoris in one. Complete atrioventricular block was the most common complication in these cases, followed by cardiogenic shock with or without right ventricular infarction, ventricular fibrillation, and severe sinus arrest. These complications were corrected with intravenous fluid, intravenous atropine or cardiac defibrillation. During a median follow-up period of 26 months, none of the patients expired or suffered nonfatal reinfarction. Two individuals who did not stop smoking during follow-up developed recurrent angina after self-discontinuation of calcium antagonists. Conclusions Coronary Vasospasm can be a cause of life-threatening cardiac arrhythmias in patients with acute Coronary syndrome and no hemodynamically significant Coronary artery disease. Coronary angiography with/without intra-Coronary ergonovine testing is necessary in acute Coronary syndrome patients to identify the underlying pathology and establish appropriate treatment in these cases.
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Coronary Vasospasm as a possible cause of elevated cardiac troponin i in patients with acute Coronary syndrome and insignificant Coronary artery disease
American Heart Journal, 2002Co-Authors: Chaohung Wang, Mingjui Hung, Litang Kuo, Wenjin CherngAbstract:Abstract Background Abnormal levels of serum cardiac troponin I (cTnI) are occasionally found in patients presenting with acute Coronary syndromes but having insignificant Coronary artery disease. Before one concludes that an abnormal cTnI level is a false-positive result, the possibility of Coronary Vasospasm should be considered. This study investigated whether Coronary Vasospasm could be a reason for elevated cTnI in this patient population. Methods and Results This investigation enrolled 93 patients who presented to the emergency department with suspected Coronary ischemia and had insignificant Coronary artery disease. cTnI was elevated in 23 patients (25%) and was normal in 70 patients (75%). Coronary Vasospasm, documented by an ergonovine provocation test, was found in 38 patients (41%). Patients with elevated cTnI levels, compared with those with normal cTnI, were older (63 ± 13 y vs 56 ± 14 y, P =.032), had a higher incidence of males (78% vs 52%, P =.049) and positive ergonovine provocation tests (74% vs 30%, P
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cardiopulmonary resuscitation during Coronary Vasospasm induced by tilt table testing
Pacing and Clinical Electrophysiology, 2000Co-Authors: Chaohung Wang, Mingjui Hung, Wenjin CherngAbstract:A 65-year-old man presented to our institution with recurrent episodes of early morning chest discomfort and near syncope. An ergonovine provocation test documented a diagnosis of Coronary va-sospastic angina. During our investigation of the syncope, a head-up tilt table test provoked a severe episode of Coronary Vasospasm that resulted in a life-threatening cardiac event. The present case reminds us that an elevation of ST segments on the electrocardiogram during tilt testing should be promptly managed as an attack of Coronary Vasospasm.
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Coronary Vasospasm induced during isoproterenol head up tilt test
American Journal of Cardiology, 1997Co-Authors: Chaohung Wang, Wenjin CherngAbstract:C spasm has been reported to be related to syncope and sudden death.1 The head-up tilt test is known as a useful method in the evaluation of syncope of unknown origin.2 No report has shown that the tilt test can provoke Coronary spasm. We present 3 cases in which Coronary spasm was induced during an isoproterenol tilt-table test and discuss the mechanism. • • • CASE 1: A 47-year-old man was admitted for workup of recurrent syncope, which followed chest tightness in the early morning. Physical examination, resting 12lead electrocardiogram, chest xray, echocardiogram, and biochemistry were normal. Exercise stress testing did not provoke an ischemic response and his Coronary angiogram showed normal Coronary arteries. Then, a tilt test was performed with an isoproterenol infusion at doses of 1, 2, and 3 mg/min at each stage including supine and 70° head-up tilt for 6 minutes. The baseline heart rate was 59 beats/min. After progressively increasing the dose of isoproterenol to 3 mg/min for 6 minutes, his heart rate increased a little to 61 beats/ min with a blood pressure of 96/48 mm Hg. Five minutes after head upright tilting with a 3 mg/min isoproterenol infusion, blood pressure and heart rate increased to 109/54 mm Hg and to 90 beats/min respectively, and meanwhile, a progressive elevation in the ST segment in multiple leads was also noted (Figure 1). The initial ST-segment elevation was found in leads II, III, and aVF, subsequently shifting to leads I, aVL, and precordial leads V1 to V6. Thereafter, chest tightness developed with marked hypotension (blood pressure 58/34 mm Hg). These conditions resolved after lying down and after sublingual nitroglycerin was administered. Electrocardiographic abnormalities returned to normal completely after 24 hours. Holter monitoring documented transient ST-segment elevation with nonsustained ventricular tachycardia at 1:30 A.M. (Figure 2). After treatment with nifedipine and isosorbide nitrate, this patient was free of chest pain and syncope, and no more ST-segment changes were induced by repeat tilt test. CASE 2: A 65-year-old man had 4 episodes of near syncope following typical chest discomfort in the morning. Resting electrocardiogram and Coronary angiogram were normal. A tilt test were performed with a blood pressure of 115/85 mm Hg and a heart rate of 78 beats/min at baseline. During From the Cardiology Section, Department of Medicine, Chang Gung Medical College, Chang Gung Memorial Hospital, Keelung, Taiwan. Dr. Cherng’s address is: Chang Gung Memorial Hospital, 222 Mai Chin Road, Keelung, Taiwan. Manuscript received June 12, 1997; revised manuscript received and accepted September 5, 1997. FIGURE 1. Twelve-lead electrocardiogram (Case 1) showing ST-segment elevation in leads II, III, and aVF after a 5-minute head-up tilt with an isoproterenol infusion at a rate of 3 mg/min. ST elevation migrated to leads I, aVL, and V1 to V6 8 minutes later with complete resolution after 24 hours.
Deborah Tepper - One of the best experts on this subject based on the ideXlab platform.
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qt prolongation torsade de pointes myocardial ischemia from Coronary Vasospasm and headache medications part 1 review of serotonergic cardiac adverse events with a triptan case
Headache, 2013Co-Authors: Mark J Stillman, Stewart J Tepper, Deborah TepperAbstract:Serotonin (5-hydroxytryptamine)1B/1D agonists are vasoconstrictors that can affect Coronary and cerebral arteries. Retrosternal chest, arm, and jaw pain following triptan use is generally attributed to “triptan sensations” and dismissed as noncardiac. However, triptans narrow normal Coronary arteries and occasionally trigger Vasospasm. They are contraindicated in atherosclerotic vascular disease. Part 1 of this review examines the relationship of medications used in migraine with the likelihood of causing Vasospasm or vasoconstriction, and the triggering of cardiac arrhythmias. We report an illustrative case of polymorphic ventricular tachyarrhythmia, electrocardiogram changes consistent with cardiac ischemia, and acquired corrected QT interval lengthening following oral sumatriptan in a 53-year-old migraineur without risk factors for Coronary artery disease (CAD). Extensive evaluation revealed insignificant single Coronary vessel atherosclerosis and Coronary artery Vasospasm on ergonovine challenge. The report highlights the hidden risk that may underlie a “triptan sensation” and the possible association of the vasospastic features of Raynaud's phenomenon, migraine headaches, and Coronary Vasospasm. Part 1 discusses the risks for Torsade de Pointes, Vasospasm, and ischemia, with a review and discussion of case reports of triptan-associated cardiovascular events in migraineurs with and without CAD risk factors or documented CAD; of the epidemiology and studies of triptans, Vasospasm, and cardiovascular morbidity; and of the relationship of variant angina, migraine, and vasospastic disease. In the second part of this review, headache medications and their propensity for corrected QT prolongation will be summarized.
Kevin Alford - One of the best experts on this subject based on the ideXlab platform.
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cardiac arrest in a young man following excess consumption of caffeinated energy drinks
The Medical Journal of Australia, 2009Co-Authors: Adam J Berger, Kevin AlfordAbstract:An otherwise healthy 28-year-old man had a cardiac arrest after a day of motocross racing. He had consumed excessive amounts of a caffeinated "energy drink" throughout the day. We postulate that a combination of excessive ingestion of caffeine- and taurine-containing energy drinks and strenuous physical activity can produce myocardial ischaemia by inducing Coronary Vasospasm.
Michael H Wall - One of the best experts on this subject based on the ideXlab platform.
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rocuronium induced Coronary Vasospasm kounis syndrome
International Journal of Cardiology, 2009Co-Authors: Richard E Fagley, Alejo Visuara, Anna Woodbury, Michael H WallAbstract:A 49-year-old male became hypotensive, bradycardic, and suffered myocardial injury during induction of anesthesia with lidocaine, propofol, and rocuronium in the operating room. Coronary arteriography revealed Coronary Vasospasm in Coronary arteries otherwise free of disease. In the ICU, the patient was again administered rocuronium for a procedure with subsequent hypotension, bradycardia, and ST elevation on telemetry that resolved with administration of diphenhydramine and hydrocortisone. An allergic reaction to rocuronium with Coronary Vasospasm is suspected, suggestive of the Type 1 variant of Kounis syndrome. This is the first report to describe a case of rocuronium-induced Type 1 Kounis syndrome.
