We applaud the authors of "Invasive Evaluation of Patients With Angina in the Absence of Obstructive Coronary Artery Disease," 1 who demonstrated an occult coronary abnormality in more than three quarters of these patients. Identifying the underlying abnormality is especially important for potentially life-threatening conditions that are amenable to treatment such as coronary artery spasm. Coronary spasm is associated with myocardial infarction, arrhythmias, and sudden death yet is responsive to calcium channel blockers and nitrates. Surprisingly, as stated in the accompanying editorial,2 no patient had inducible spasm on acetylcholine provocation. This observation warrants closer scrutiny, particularly in relation to the acetylcholine provocation method used.. Intracoronary acetylcholine administration is used to assess the presence of coronary endothelial function and coronary spasm. Its use is ideal, given its very short half-life and established safety record.. Endothelial function studies ...
Symptoms are often very similar to pain associated with a more typical heart attack (development of a blockage in a heart artery). Symptoms often occur at rest, and at night. This is different than typical chest pain associated with heart artery blockages which is more typically experience during exertion.. ...
Vasospastic angina is caused by sudden occlusive vasoconstriction of a segment of an epicardial artery, which can present with a wide spectrum of clinical scenario. We report the cases of two patients diagnosed with vasospastic angina, with one of which presenting with sudden cardiac arrest, while the other presenting with a relatively benign syncope. But both of them have J waves formation on ECG during active ischemia. The diagnosis and management of vasospastic angina, as well as the proposed clinical significance of J waves during coronary spasm are discussed. ...
Coronary artery spasm is a cause of myocardial infarction with non-obstructive coronary arteries (MINOCA). Coronary spasm may occur spontaneously or in response to prescribed or illicit drugs. Myocardial injury and cardiomyopathies have been reported in association with the use of stimulants in children and adults with attention deficit hyperactivity disorder (ADHD).
In this issue of the Journal, Ong et al. (1) sought to determine the prevalence of coronary spasm in angina patients with angiographically normal coronary arteries. Of 304 patients with stable angina, 144 (47%) had normal coronary arteries or only minimal irregularities (,20% diameter reduction) at coronary angiography. Acetylcholine (ACH) testing was performed in 124 of the 144 patients and provoked coronary spasm in 77 (62%). Thirty-five patients (45%) with constrictor response presented with epicardial spasm (defined as a ≥75% diameter reduction with reproduction of the symptoms of the patient), and 42 patients (55%) presented with microvascular spasm (defined as ischemic electrocardiographic changes with symptom reproduction, but no epicardial spasm). Overall two-thirds of patients undergoing the ACH test presented with abnormal coronary artery vasomotion, a finding that also confirmed the presence of the ischemic syndrome.. The authors are to be congratulated for attempting to determine ...
Definitive diagnosis of coronary artery spasm often begins with a coronary angiogram that is performed with the expectation of finding atherosclerotic narrowing of a heart artery. Patients with coronary artery disease may have one or more plaques in their coronary arteries and unless the blockages are severe, there may be no symptoms. Two patients had coronary artery disease, and three had angiographically normal coronary arteries.. Acting fast at the first sign of heart attack symptoms can save your life and limit damage to your heart. Whether you have had a heart attack or not, if you feel depressed, tell your doctor. You can even have a silent heart attack, one with no symptoms. The symptoms of a heart attack can vary from person to person. To prevent a heart attack, you will most likely need to make lifestyle changes. The patient may need to be hospitalized to prevent a heart attack.. Without normal blood flow from the coronary arteries the heart becomes lack of oxygen and vital nutrients ...
1. Armstrong PW. Stable ischemic syndromes. In: Topol E. Textbook of Cardiovascular Medicine. Philadelphia: Lippincott Raven Publishers 1998. 2. Chatterjee T, Juelke PD, Thum P et al. Successful brachytherapy of coronary vasospasm. Heart 2003; 89(9): 25. 3. Cheng TO. Clinical implication of the hyperventilation test in the diagnosis of coronary artery spasm. Am J Cardiol 1997; 80: 1647. 4. Gersh BJ, Braunwald E, Bonow BO. Chronic coronary artery disease. In: Braunwald E. Heart Disease. A textbook of cardiovascular medicine. 6th ed. Philadelphia: WB Saunders 2001. 5. Halawa B, Salomon P. Activity of transmembrane calcium transport and levels of endothelin-1 in patients with variant angina. Pol Arch Med Wewn 2000; 104(2): 447-453. 6. Hirano Y, Ozasa Y, Yamamoto T et al. Hyperventilation and cold pressor stress echocardiography for noninvasive diagnosis of coronary artery spasm. J Am Soc Echocardiogr 2001; 14(6): 626-633. 7. Hirano Y, Ozasa Y, Yamamoto T et al. Diagnosis of vasospastic angina by ...
Coronary artery spasm (CAS) is an established cause for anginal chest pain, the cardinal symptom of myocardial ischaemia, in patients with angiographically unobstructed coronary arteries. Evidence from large clinical studies has revealed that about 50% of patients undergoing diagnostic coronary angiography for suspected coronary artery disease (CAD) had either normal or near
Exercise induced ST elevation in patients with previous myocardial infarction may simply indicate left ventricular wall asynergy. ST segment elevation without prior myocardial infarction is a rare condition and is commonly associated with critical coronary artery stenosis.1 Temporary ST segment elevation associated with chest pain is the hallmark of variant (Prinzmetal) angina, and is a consequence of severe coronary spasm. In a way that is not yet fully understood, exercise can induce coronary spasm in patients with variant angina, as demonstrated in small groups of patients subjected to supine bicycle exercise on the cardiac catheterisation table.2DSE is widely performed as a useful diagnostic tool in patients with known or suspected coronary artery disease. Through its inotropic and chronotropic effects, dobutamine increases the myocardial oxygen demand and may induce ischaemia and segmental wall motion abnormality in the presence of significant coronary artery disease. Myocardial ischaemia ...
There have been rare reports of serious cardiac adverse reactions, including acute myocardial infarction, occurring within a few hours following administration of SUMAVEL® DosePro®. SUMAVEL® DosePro® may cause coronary artery vasospasm (Prinzmetals angina). These types of reactions have occurred in some patients without known CAD. For triptan-naïve patients with multiple cardiovascular risk factors who have a negative cardiovascular evaluation, consider administrating the first SUMAVEL® DosePro® dose in a medically-supervised setting and performing an electrocardiogram (ECG) immediately following SUMAVEL® DosePro® administration. For such patients, consider periodic cardiovascular evaluation in intermittent long-term users of SUMAVEL® DosePro®. Life-threatening arrhythmias have been reported within a few hours following the administration of 5-HT1 agonists. Discontinue SUMAVEL® DosePro® if these disturbances occur. Sensations of tightness, pain, pressure, and heaviness have been ...
The mean oral absolute online bioavailability of sales the maxalt retinal detachment symptoms Tablet is retin about online 45, and how to get retin a retin mean peak plasma concentrations (Cmax) are reached in sales approximately 1-1.5 hours (Tmax). Diagnosis Your health care provider may check the size of sales your sales prostate gland directly by putting a sales gloved finger in your rectum and feeling the back wall of the prostate. You can retin ask your pharmacist or sales doctor for information about maxalt that is written for health professionals. Have shortness of breath or chest pain. If there is evidence of CAD or coronary artery vasospasm, maxalt should not be retin administered see contraindications. This medication may be available under multiple brand names and/or in several different forms. You can place the order online, by mail, online by fax or toll-free over the telephone. Your health care provider will also order blood tests, and possibly a sales urine sample. Free Make Up ...
METHODS AND RESULTS Injury was induced by inflation of a balloon catheter 50 +/- 6% above baseline arterial diameter; dogs were followed for 2 hours before death. Epicardial coronary diameters at arteriography and extent of thrombus deposition at serial histological sections were analyzed in controls (n = 20) and in dogs pretreated with superoxide dismutase (SOD, a superoxide radical scavenger, n = 10); other dogs were pretreated with the hydrogen peroxide scavenger catalase (n = 8), the iron chelator deferoxamine (n = 6), or the hydroxyl radical scavenger 1,3-dimethyl-2-thiourea (n = 9). Angioplasty-induced injury was similar among groups. After angioplasty, control dogs exhibited localized and persistent vessel constriction, which was maximal at the initial 5 minutes (28.9 +/- 6.3% diameter decrease versus baseline). Corresponding arterial diameters of SOD-treated dogs were 24-69% larger (95% confidence interval, p less than 0.001) than controls at 5 minutes and, on average, 32% larger than ...
If patients could recognise themselves, or anyone else could recognise a patient from your description, please obtain the patients written consent to publication and send them to the editorial office before submitting your response [Patient consent forms] ...
Rev Esp Cardiol. 1997 Nov;50(11):808-11. [The placement of a Wiktor stent for the treat ment of vasospastic angina: a case report]. [Article in Spanish] Rodríguez Díez S1, Lázaro R, Ruiz Nodar JM, Enero J, Romero C, Gómez Recio M, Martínez Elbal L.
I am a 43 yo female who had a heart attack. My only risk factor is high bp due to kidney surgery as a child that has been controlled by meds. My EKG indicated damage and I had troponin levels of 6 and ...
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Impaired coronary microvascular dilatory function can lead to exercise induced myocardial ischemia and angina pectoris even in patients without significant (|50%) obstructive coronary atherosclerosis (APWOCA). Diffuse distal vessel epicardial spasm a
Dr. Stern responded: Yes it can in some. If you are prone to coronary artery spasm, then emotional |a href="/topics/stress" track_data="{
In patients with angina and nonobstructive coronary-artery disease, coexistence of epicardial coronary spasm and increased microvascular resistance (IMR) is associated with worse outcomes, according to Japanese researchers.
how do you think this case could have played out differently? Think very few providers would get their cardiologists to bite on young, intoxicated male c/o chest pain with that initial ekg. Im sure most would write it off to early repol. maybe with serial ekgs or echo, but even then itd be a tough sell. Even more concerning is that we all see quite a few intoxicated and agitated young males/females in the department daily. Similar presentations. Feel as though we are so prone to write it off as demand ischemia, coronary vasospasm, trop leak etc.. in this population ...
how do you think this case could have played out differently? Think very few providers would get their cardiologists to bite on young, intoxicated male c/o chest pain with that initial ekg. Im sure most would write it off to early repol. maybe with serial ekgs or echo, but even then itd be a tough sell. Even more concerning is that we all see quite a few intoxicated and agitated young males/females in the department daily. Similar presentations. Feel as though we are so prone to write it off as demand ischemia, coronary vasospasm, trop leak etc.. in this population ...
PDE5 takes part in many physiological and pathological functions, therefore selective PDE5 inhibitors are potentially useful for a variety of pathologies. At the present, PDE5 inhibitors available on the market have been used for the treatment of erectile dysfunction but, at the same time, are in clinical trials investigating other pathologies such as pulmonary arterial hypertension, coronary vasospasm, benign prostatic hyperplasia etc. This review analyzes the PDE5 inhibitors currently in clinical use, the drugs in clinical trials and the most representative chemical classes published in literature in this last decade ...
Introduction Oral capecitabine is an oral prodrug of 5-fluorouracil that has been integrated into the management of multiple cancer types because of the convenience of administration and its efficacy...
Procardia belongs to a class of medications called calcium channel blockers. These medications block the transport of calcium into the smooth muscle cells lining the coronary arteries and other arteries of the body. Since calcium is important in muscle contraction, blocking calcium transport relaxes artery muscles and dilates coronary arteries and other arteries of the body. By relaxing coronary arteries, procardia is useful in treating and preventing chest pain (angina) resulting from coronary artery spasm. Relaxing the muscles lining the arteries of the rest of the body lowers the blood pressure, which reduces the burden on the heart as it pumps blood to the body. Reducing heart burden lessens the heart muscles demand for oxygen, and further helps to prevent angina in patients with coronary artery disease ...
Procardia belongs to a class of medications called calcium channel blockers. These medications block the transport of calcium into the smooth muscle cells lining the coronary arteries and other arteries of the body. Since calcium is important in muscle contraction, blocking calcium transport relaxes artery muscles and dilates coronary arteries and other arteries of the body. By relaxing coronary arteries, procardia is useful in treating and preventing chest pain (angina) resulting from coronary artery spasm. Relaxing the muscles lining the arteries of the rest of the body lowers the blood pressure, which reduces the burden on the heart as it pumps blood to the body. Reducing heart burden lessens the heart muscles demand for oxygen, and further helps to prevent angina in patients with coronary artery disease ...
Your doctor may prescribe medications such as nitroglycerin to relax the coronary arteries, calcium antagonists to guard against coronary artery spasm , or aspirin and other antiplatelet drugs to prevent blood clots in the area of the blockage. If you have a stent, you will have to take blood thinners (such as aspirin) inde?nitely. You will also take an antiplatelet such as clopidogrel at least one month after a bare-metal stent is placed in your artery and two or more years after a drug-eluting stent is placed in your artery. Because of the presence of the metal stent, you should not have magnetic resonance imaging (MRI) for at least 4 weeks with- out checking with your doctor ?rst. But you can go through a metal detector at an airport without a problem.. Restenosis. Restenosis (renarrowing or constriction) can occur in the same area of the blood vessel where your angioplasty was done, often within about 6 months of the original procedure. Although placement of a stent greatly reduces the ...
Jen Woodall wrote: , I strongly believe , that should be recognized in whatever way each person chooses. I always , acknowledge the date (well, close to it--cant always remember the exact , date) of my dx in some way. I know my diagnosis date EXACTLY, and I know exactly when my BGs started to go up, and I know when they went kablooie rapidly. I started to have problems in the summer of 1991; my BGs went kablooie starting on July 28, 1992, and I was officially diagnosed on Aug. 17, 1992 after landing in the hospital with a coronary artery spasm. Then they went back down again, and I was able to maintain on diet and exercise until the summer of 1993; in Sept. 1993, I went to the doc, and my BGs were once again rising rapidly, so she tried increasing doses and different sulfonylureas to no effect. I finally went on insulin on May 12, 1994, and THATs the date I celebrate! Like insulin gave me my life back, and I think THATs worth celebrating -- during my time on diet and orals, I was consistently ...
Coronary artery spasm is an important pathogenetic mechanism in some forms of myocardial ischemic disease. Factors that may be important in the genesis of spasm include the autonomic nervous system, prostaglandins, endoperoxides, thromboxanes, and the calcium availability to the contractile apparatus. Spasm results in myocardial ischemia with attendant chest pain and electrocardiographic and hemodynamic changes; it is the primary pathogenetic mechanism in Prinzmetals variant angina and has been found in association with classic angina pectoris and acute myocardial infarction. Diagnosis of coronary artery spasm is firmly made only by coronary angiography. Treatment includes the use of both short- and long-acting nitrates and the slow-channel blocking agents such as verapamil, nifedipine, and perhexiline. ...
TY - JOUR. T1 - Long-Term Prognosis of Vasospastic Angina without Significant Atherosclerotic Coronary Artery Disease. AU - Egashira, Kcnsuke. AU - Kikuchi, Yutaka. AU - Sagara, Tomohiko. AU - Sugihara, Masayoshi. AU - Nakamura, Motoomi. PY - 1987/1/1. Y1 - 1987/1/1. N2 - Long-term prognosis of 90 patients with vasospastic angina without significant coronary artery disease (less than 50% reduction in luminal diameter) was examined for a mean follow-up period of 4 years. All patients had episodes of angina at rest and were treated with calcium antagonists. One patient developed myocardial infarction and 2 died suddenly during the follow-up period. In the patient with myocardial infarction, there was an abrupt worsening of angina prior to the infarction despite therapy with a calcium antagonist. One of the sudden death patients discontinued his calcium antagonist before his death. Of the sudden death patients, one had ventricular tachycardia and the other had a complete atrioventricular block ...
Treatment in the emergency department should focus on frequent evaluation (e.g. every 2 hours) of the patients respiratory status with serial FVC and NIF and intubating promptly at signs of respiratory failure. Sitting the patient upright may help temporize the patients dyspnea while preparing for intubation. Even if not intubated, patients presenting with myasthenic crises will need admission to the ICU. First line therapies include IVIG and plasmapheresis, both of which take several days to reach full clinical effect by removing acetylcholine receptor antibodies from the circulation. High dose glucocorticoid therapy and other immunosuppresants such as azathioprine and cyclosporine can be initiated but are intended as long-term therapies and do not provide any benefit in the emergent setting. Anticholinesterase use, such as pyridostigmine, remains controversial because of the risk of coronary artery vasospasm (resulting in MI) and arrhythmia. A basic infectious workup, including a chest x-ray ...
Title:Rho Kinase Inhibitors: Potential Treatments for Diabetes and Diabetic Complications. VOLUME: 18 ISSUE: 20. Author(s):Hong Zhou and Yong-jun Li. Affiliation:Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, China.. Keywords:RhoA, Rho kinase, inhibitors, diabetes, complications, GTPase, hypertension, coronary vasospasm, stroke, atherosclerosis. Abstract:The small GTPase RhoA and its downstream effector, Rho kinase (ROCK), appear to mediate numerous pathophysiological signals, including smooth muscle cell contraction, actin cytoskeleton organization, cell adhesion and motility, proliferation, differentiation and the expression of several genes. Clinical interest in the RhoA/ROCK pathway has increased, due to emerging evidence that this signaling pathway is involved in the pathogenesis of several diseases, including hypertension, coronary vasospasm, stroke, atherosclerosis, heart failure and diabetes; ROCK is considered an important future ...
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Chest pain following successful percutaneous coronary interventions is a common problem. Although the development of chest pain after coronary interventions may be of benign character, it is disturbing to patients, relatives and hospital staff. Such pain may be indicative of acute coronary artery closure, coronary artery spasm or myocardial infarction, but may also simply reflect local coronary artery trauma. The distinction between these causes of chest pain is crucial in selecting optimal care.Management of these patients may involve repeat coronary angiography and additional intervention. Commonly, repeat coronary angiography following percutaneous transluminal coronary angioplasty (PTCA) in patients with chest pain demonstrates widely patent lesion sites suggesting that the pain was due to coronary artery spasm, coronary arterial wall stretching or was of non-cardiac origin. ...
Vasospastic angina is presented by myocardial ischemia with spasm of coronary artery accompanying chest pain or discomfort. The precise mechanisms have not been established, but a reduction in NO (nitric oxide) production, an imbalance between endothelium-derived relaxing and contracting factors,or an injury of endothelium have been suggested.. Impaired FMD(flow mediated endothelium-dependent vasodilation) in the brachial artery was demonstrated in vasospastic angina,and improvement of endothelial dysfunction with treatment of statin is documented in several studies.. So, we expect that statin treatment for vasospastic angina provide additional therapeutic effects via improvement of endothelial dysfunction. ...
The decades-long research focus on the pathophysiology of coronary artery disease (CAD) has provided insights into sex-specific factors that are uniquely important in the noninvasive diagnosis of myocardial ischemic syndromes in women. Evidence gained from the landmark WISE (Womens Ischemic Syndrome Evaluation) study (1) indicates that the full spectrum of CAD in women extends beyond atherosclerotic stenoses in the epicardial coronary arteries to include dysfunction of the coronary microvasculature and endothelium. Additional conditions contributing to the full pathophysiologic spectrum of acute and chronic ischemic heart disease (IHD) in women include coronary vasospasm and coronary artery dissection which mainly affect the epicardial coronary arteries and often develop in younger women (2). The implications of these diverse conditions are substantial. They create diagnostic challenges and limit the application of traditional testing strategies which, while adequate to detect obstructive ...
Acute myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Myocardial infarction occurs when myocardial ischemia, a diminished blood supply to the heart, exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms designed to maintain normal operating function and homeostasis. Ischemia at this critical threshold level for an extended period results in irreversible myocardial cell damage or death.. Critical myocardial ischemia can occur as a result of increased myocardial metabolic demand, decreased delivery of oxygen and nutrients to the myocardium via the coronary circulation, or both. An interruption in the supply of myocardial oxygen and nutrients occurs when a thrombus is superimposed on an ulcerated or unstable atherosclerotic plaque and results in coronary occlusion.1 A high-grade (,75%) fixed coronary artery stenosis caused by atherosclerosis or a dynamic stenosis associated with coronary vasospasm can also limit the supply of ...
Acute coronary syndrome (ACS) refers to acute myocardial ischemia caused by atherosclerotic coronary disease, and includes ST elevation myocardial infarction (STEMI), non-ST elevation MI (NSTEMI), and unstable angina. Cocaine accounts for up to 25% of acute MIs in people ages 18 to 45 years. [9] Qureshi AI, Suri MF, Guterman LR, et al. Cocaine use and the likelihood of nonfatal myocardial infarction and stroke: data from the Third National Health and Nutrition Examination Survey. Circulation. 2001;103:502-506. http://circ.ahajournals.org/content/103/4/502 http://www.ncbi.nlm.nih.gov/pubmed/11157713?tool=bestpractice.com The lifetime risk of nonfatal MI with cocaine use is 7 times the risk in nonusers. In the hour after cocaine is used, the risk of MI is 24 times the baseline risk. It is probably due to cocaine-induced coronary vasospasm and thrombosis, in addition to a direct effect on heart rate and arterial pressure. Cocaine also has direct myocardial toxic properties. [10] Amsterdam EA, ...
Physician researchers suspect that some cases of coronary artery spasm go unrecognized and are incorrectly treated with stents. The good news - there could be a simple fix to eliminate these unnecessary stenting procedures ...
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Nicardipine: A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.
Hello, Im a 23-year old female. I will start off by telling you when this started and what was happening. It was January of 2005, I had my 2nd child in December of 2004. I started having chest pain at...
The more of these symptoms you have, the more likely it is that youre having a heart attack. Chest pain or pressure is the most common symptom, but some people, especially women, may not notice it as much as other symptoms. You may not have chest pain at all but instead have shortness of breath, nausea, or a strange feeling in your chest or other areas.. ...
A CONTRIBUTION TO THE COMPARATIVE STUDY OF THE ORIGIN OF THE SYMPATHETIC AND THE ADRENALIN-SECRETING SYSTEMS AND OF THE VASCULAR MUSCLES WHICH THEY REGULATE. ...
Marijuana is the most commonly used psychoactive drug in the USA. A 35-year-old man with a medical history of marijuana abuse is admitted to the hospital due to crushing substernal chest pain. ECG shows evolving ST-segment elevation with a rise in cardiac enzymes, consistent with ST-elevation myocardial infarction. A urine toxicology screen is positive for cannabis and negative for cocaine and other stimulant drugs. An emergent cardiac catheterisation reveals no evidence of coronary artery disease or thrombosis. A diagnosis of coronary vasospasm is strongly considered, and the patient is started on calcium channel blocker, with a resolution of symptoms and ECG changes. Marijuana-induced coronary spasm causing myocardial infarction has rarely been reported. Marijuana is becoming a social norm in adolescents and there remains a misconception that it is harmless and even beneficial. Increasing drug abuse remains a public health concern, necessitating population education by physicians for safer ...
This syndrome was first described 100 years ago as "pseudoangina"; patients manifested chest pain, and had an abnormal stress test, but had normal coronary arteries by angiography. Kemp et al. coined the term "cardiac syndrome X" in 1973 for this clinical scenario. The incidence is higher in postmenopausal women. The underlying pathophysiology is unclear, but different authors have proposed several mechanisms. Problems with the release of endogenous vasodilators leading to spasm of the coronary arteries could be one of the reasons for this symptom complex. Therefore, women with normal coronaries are sometimes given ergonovine in the cardiac catheterization lab in order to induce coronary artery spasm and reproduce the symptoms. Another reason why these women have chest pain despite normal coronary arteries is due to "microvascular angina"-a disease of small vessels which cannot be seen clearly during cardiac catheterization, as mentioned above. overall prognosis for this group of women patients ...
MYOCARDIAL INFARCTION - death of myocardial muscle cells. - there is lack of oxygen from inadequate perfusion. CAUSES: ATHEROSCLEROSIS INADEQUATE PERFUSION TO MEET METABOLIC DEMANDS EMBOLISM OR THROMBUS CORONARY ARTERY SPASM ASSESMENT: CRUSHING, BURNING, TIGHTNESS OR SQUEEZING SUBSTERNAL PAIN LASTS THE LONGER THAN ANGINAL PAIN, USUALLY LONGER THAN 30 MINS. *IS UNRELIEVED BY REST OR…
Interpretation of coronary angiography data Fig. 15 Reproduction of a portion of a catheterization report from patient described in Fig. 10. This section reports information obtained from coronary angiography. Morphology of stenoses, percent reduction in lumen diameter, and sources of collaterization are reported. A pictorial representation of coronary arterial anatomy also is given. Coronary spasm True coronary spasm is diagnosed at the time of coronary angiography with a provocation test utilizing methylergonovine, acetylcholine, or hyperventilation. Fig. 9a-d). Any or all of these abnormalities may exist in a given patient. Compliance Compliance or distensibility is defined as the ratio of a volume change to the corresponding pressure change or as the slope of the volume-pressure ( V / P) relationship. Elastance or stiffness is the inverse of compliance ( P/ V ). Decreased compliance or increased stiffness is thus defined as an increase in the steepness of the pressure-volume plot (see Fig. ...
The purpose of this case repots are to evaluate the role of ST elevation in aVR lead and to make analysis between both cases. There are some atypical electrocardiogram (ECG) presentations which need prompt management in patient with ischemic clinical manifestation such as ST elevation in aVR lead. In this case study, we report a 68-year old woman with chief symptoms of shortness of breath and chest discomfort. She was diagnosed with cardiogenic shock, with Killip class IV, and TIMI score of 8. The second case is a 57-year-old man with typical chest pain at rest which could not be relieved with nitrate treatment ...
We would like to thank Dr. Ratib and colleagues for taking interest in our recently published article (1). We completely agree and have also shown that coated sheaths reduce radial artery spasm and the discomfort experienced by the patient during transradial procedures. Procedural success rates are high with accumulated experience and improvement in equipment.. In our study, clinical evidence of radial artery spasm was observed in 19% of the patients in the coated group and 39% in the uncoated group. We have used a liberal clinical definition to diagnose spasm and avoided the routine use of vasodilators to abolish its potential impact on our end points. This is consistent with the clinical practice of the investigators. All procedures were performed by experienced radial operators using 6-F sheaths.. Spasm resulted in procedural failure in only 17 (2.1%) cases, and in the majority of cases, the procedure was completed successfully via the contralateral radial artery. As suggested, Dham et al. ...