Pathological Q-Waves With Coronary Artery Spasm.
Ontology highlight
ABSTRACT:
SUBMITTER: Hirota Y
PROVIDER: S-EPMC8302779 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:INTRODUCTION:Postoperative coronary artery spasm is an infrequent life-threatening event after cardiac surgery which can occur without an underlying coronary disease PRESENTATION OF CASE:We report a documented case of a 67-year-old man with normal coronary arteries submitted to mitral valve replacement. Immediately after surgery he had a ST elevation in the inferior leads, and an inferior wall hypokinesia at the trans-oesophageal echo. A coronary angiography demonstrated a focal spasm in the right coronary artery which was successfully treated by intracoronary injection of nitrates. The following postoperative course was uneventful and the left ventricular function returned to normal. DISCUSSION:A coronary artery spasm should be suspected whenever a postoperative infarction occurs after valvular surgery especially in absence of associated coronary artery disease. In this cases postoperative coronary angiography allows both the diagnosis and the treatment. CONCLUSION:This case-report summarizes the findings of this rare and potentially life-threatening cause of early postoperative ischemia and highlights the role of early coronary angiography in the cases of suspected myocardial infarction after cardiac surgery.
| S-EPMC4353950 | biostudies-literature
Project description:Coronary artery spasm (CAS) plays an important role in the pathogenesis of ischemic heart disease, including angina pectoris, myocardial infarction, and sudden death, occurring most often from midnight to early morning. CAS is prevalent among East Asians and is associated with an aldehyde dehydrogenase 2 (ALDH2)-deficient genotype (ALDH2*2) and alcohol flushing, which is prevalent among East Asians but is virtually non-existent in other populations. ALDH2 eliminates not only acetaldehyde but also other toxic aldehydes from lipid peroxidation and tobacco smoking, thereby protecting tissues and cells from oxidative damage. Risk factors for CAS include smoking and genetic polymorphisms including those of ALDH2*2, endothelial NO synthase, paraoxonase I, and interleukin-6. Accordingly, oxidative stress, endothelial dysfunction, and low-grade chronic inflammation play an important role in the pathogenesis of CAS, leading to increased coronary smooth muscle Ca2+ sensitivity through RhoA/ROCK activation and resultant hypercontraction. Ca-channel blockers blocking the intracellular entry of Ca2+ are specifically effective for treatment for CAS.
| S-EPMC6403432 | biostudies-literature
Project description:BACKGROUND:Coronary artery spasm (CAS) and stress cardiomyopathy (SC) have different characteristic clinical manifestations in the case of suspicious myocardial infarction with nonobstructive coronary arteries. Established recurrence rates of both conditions have been reported, however, alternate recurrent CAS and SC in the same individual have not been described. CASE PRESENTATION:A 59-year-old man suffered from atypical chest pain in the first episode, acute heart attack in the second and third episodes (totally 3 times over a period of approximately 5 years). During the first episode, he visited our hospital with mild paroxysmal chest pain without obvious inducement for approximately 2 years. He was underdiagnosed at that time without other obvious findings except the poor R wave progression in V1-3 leads revealed in electrocardiogram. At 4 months after the first episode, he suffered from a heart attack (the second episode) and was diagnosed with SC based on the coronary angiography (CAG) and left ventriculography findings of nonobstructive coronary arteries combined with a classic apical ballooning shape. At 31 months after the second episode, he suffered another heart attack (the third episode) and was diagnosed with CAS based on the CAG results of recoverable severe multivessel stenoses. During the episodes, partial reversible nature of apical hypokinesis was observed in echocardiogram. In retrospect, the patient suffered silent CAS in the first episode, SC in the second episode, and severe multivessel CAS in the third episode. CONCLUSION:The unusual presentations observed in this case have not been reported. This case suggests that cardiologists should be aware of the possibility of alternate recurrent CAS and SC in the same individual. Provocative tests for spasm and cardiac magnetic resonance imaging might help gain more insights into this issue.
| S-EPMC7641797 | biostudies-literature
Project description:Background Coronary artery spasm plays a vital role in the pathogenesis of coronary plaques. We sought to investigate the plaque characteristics of co-existing organic lesions in patients with coronary artery spasm in comparison to those without coronary artery spasm by intracoronary optical coherence tomography (OCT). Methods and Results We included 39 patients who presented with a symptom suspected of coronary spastic angina and had an organic lesion, defined as ≥plaque burden of 50% assessed by OCT. Coronary artery spasm was diagnosed by positive acetylcholine provocation test, or by spontaneous spasm detected during coronary angiography. A total of 51 vessels with an organic lesion were identified. Of these, coronary artery spasm was observed in 30 vessels (spasm), while not in 21 vessels (non-spasm). Organic lesions in the spasm vessels, compared with those in the non-spasm vessels, had a higher prevalence of layered plaque (93% versus 38%, P<0.001), macrophages (80% versus 43%, P=0.016), and intraplaque microchannels (73% versus 24%, P<0.001), and lower prevalence of macrocalcification (23% versus 62%, P=0.009) as assessed by OCT. Conclusions Layered plaque, macrophages, and intraplaque microchannels, were frequently observed in organic lesions in patients with coronary artery spasm. These findings suggest that coronary artery spasm induces local thrombus formation as well as active inflammatory response, therefore increasing the risk of rapid plaque progression and ischemic events in patients with coronary artery spasm.
| S-EPMC9075431 | biostudies-literature
Project description:BackgroundVentricular arrhythmia and sudden cardiac arrest caused by multivessel coronary artery spasm (CAS) is rare. Although coronary angiography (CAG) with provocation testing is the diagnostic gold standard in current vasospastic angina guidelines, it can cause severe procedure-related complications. Here, we report a novel technique involving dual-acquisition coronary computed tomography angiography (CCTA) to detect multivessel CAS in a patient who survived out-of-hospital cardiac arrest (OHCA).Case summaryA 58-year-old healthy Korean male survived OHCA caused by ventricular fibrillation (VF), experiencing seven episodes of defibrillation and cardiopulmonary resuscitation, and was referred to the Emergency Room. Vital signs were stable and physical examination, electrocardiogram, chest, and brain CT did not show any abnormal findings, except elevated hs-Troponin I levels (0.1146 ng/mL). Echocardiogram revealed a regional wall motion abnormality in the inferior wall, with a low normal left ventricular ejection fraction (50%). A multivessel CAS (both left and right) was detected using a dual-acquisition CCTA technique (presence and absence of intravenous nitrate). During CAG with the 2nd injection of ergonovine, a prolonged and refractory total occlusion in the proximal-ostial right coronary artery was completely relieved after a seven-cycle intracoronary injection regimen of nitroglycerine. The patient was discharged with the recommendation of smoking and alcohol cessation. Nitrate and calcium channel blockers were also prescribed. The patient had no further events at 3 months of follow-up after discharge.DiscussionDual-acquisition CCTA is a promising tool to detect multivessel CAS.
| S-EPMC7793155 | biostudies-literature
Project description:BackgroundCoronary artery spasm is an established mechanism of myocardial infarction with non-obstructive coronary arteries (MINOCA). Various mechanisms have been proposed, ranging from vascular smooth muscle hyperreactivity to endothelial dysfunction, to autonomic nervous system dysregulation.Case summaryWe report a case of a 37-year-old woman who presented with recurrent non-ST elevation myocardial infarction (NSTEMI), coinciding with her menstrual periods. Intracoronary acetylcholine provocation testing resulted in coronary spasm in the left anterior descending artery (LAD) that was relieved with nitroglycerine. Initiating calcium channel blockade and suppressing cyclical variation in sex hormones resulted in improvement of her symptoms and cessation of monthly NSTEMI events due to coronary spasm.DiscussionInitiating calcium channel blockade and suppressing cyclical variation in sex hormones resulted in improvement of her symptoms and cessation of monthly NSTEMI events due to coronary spasm. Catamenial coronary artery spasm is a rare, but clinically important, presentation of myocardial infarction with non-obstructive coronary arteries (MINOCA).
| S-EPMC9924495 | biostudies-literature
Project description:Coronary spasm may present as acute coronary syndrome (ACS), "which can be an ST segment elevation myocardial infarction (STEMI), non-STEMI, or unstable angina." However, the prevalence of coronary spasm in patients with ACS remains unknown due to scarcity of data. Concomitant coronary spasm may mask the true atherosclerosis burden in such cases, posing several management challenges. We illustrate the case of managing an ACS patient with concomitant spasm and atherosclerotic disease. We show that the routine use of vasodilator treatment in ACS cases may prevent inappropriate stenting by identifying concomitant coronary spasm, influencing the clinical outcomes associated with inappropriate stenting in the setting of coronary spasm.
| S-EPMC3699217 | biostudies-other
Project description:Coronary artery spasm (CAS) is considered an important mechanism of acute coronary syndrome but not very common in the clinical setting. We report a case of a 42-year-old woman with chest pain lasting for 4 h due to diffuse CAS, which led to widespread ST-segment elevation in multiple leads of the electrocardiogram and elevated cardiac troponin T. Emergency coronary angiography at admission showed significantly different morphological results from the second angiography during hospitalization, indicating the patient's discomfort was due to CAS rather than stenosis. Our case illustrates that diffuse CAS can cause widespread ST-segment elevation and severe ACS.
| S-EPMC8411782 | biostudies-literature
Project description:Coronary artery spasm (CAS) plays an important role in the pathogeneses of various ischemic heart diseases and has gradually become a common cause of life-threatening arrhythmia. The specific molecular mechanism of CAS has not been fully elucidated, nor are there any specific diagnostic markers for the condition. Therefore, this study aimed to examine the specific molecular mechanism underlying CAS, and screen for potential diagnostic markers. To this end, we successfully constructed a rat CAS model and achieved in vitro culture of a human coronary-artery smooth-muscle cell (hCASMC) contraction model. Possible molecular mechanisms by which protein kinase C (PKC) regulated CAS through the C kinase-potentiated protein phosphatase 1 inhibitor of 17 kDa (CPI-17)/myosin II regulatory light chain (MLC2) pathway were studied in vivo and in vitro to screen for potential molecular markers of CAS. We performed hematoxylin and eosin staining, myocardial zymogram, and transmission electron microscopy to determine myocardial and coronary artery injury in CAS rats. Then, using immunohistochemical staining, immunofluorescence staining, and Western blotting, we further demonstrated a potential molecular mechanism by which PKC regulated CAS via the CPI-17/MLC2 pathway. The results showed that membrane translocation of PKCα occurred in the coronary arteries of CAS rats. CPI-17/MLC2 signaling was observably activated in coronary arteries undergoing CAS. In addition, in vitro treatment of hCASMCs with angiotensin II (Ang II) increased PKCα membrane translocation while consistently activating CPI-17/MLC2 signaling. Conversely, GF-109203X and calphostin C, specific inhibitors of PKC, inactivated CPI-17/MLC2 signaling. We also collected the coronary artery tissues from deceased subjects suspected to have died of CAS and measured their levels of phosphorylated CPI-17 (p-CPI-17) and MLC2 (p-MLC2). Immunohistochemical staining was positive for p-CPI-17 and p-MLC2 in the tissues of these subjects. These findings suggest that PKCα induced CAS through the CPI-17/MLC2 pathway; therefore, p-CPI-17 and p-MLC2 could be used as potential markers for CAS. Our data provide novel evidence that therapeutic strategies against PKC or CPI-17/MLC2 signaling might be promising in the treatment of CAS.
| S-EPMC10932290 | biostudies-literature
Project description:Acute vasospastic angina, formerly known as Prinzmetal angina, is characterized by transient electrocardiographic changes that are not related to exertion. Its atypical presentation makes it difficult to establish the diagnosis, so it is probably underrecognized and therefore mismanaged. We treated a 49-year-old woman who presented with a 2-day history of chest pain associated with palpitations. Abnormal radionuclide stress test results prompted diagnostic coronary angiography, during which the patient reported chest pain and became hemodynamically unstable. Active coronary vasospasm at multiple sites was treated with intracoronary nitroglycerin and nicardipine, leading to immediate recovery. Our case highlights the importance of accurate, timely diagnosis of vasospastic angina, and of early recognition and management of spontaneous coronary spasm during angiography.
| S-EPMC9053660 | biostudies-literature