Successful detection of supraventricular tachycardia following ST elevation due to vasospastic angina using an insertable cardiac monitor in a patient with recurrent syncope: a case report.
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SUBMITTER: Kasai Y
PROVIDER: S-EPMC10633680 | biostudies-literature | 2023 Nov
REPOSITORIES: biostudies-literature
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Successful detection of supraventricular tachycardia following ST elevation due to vasospastic angina using an insertable cardiac monitor in a patient with recurrent syncope: a case report.
Kasai Yuhei Y Morita Junji J Kitai Takayuki T Fujita Tsutomu T
European heart journal. Case reports 20231009 11
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Project description:BackgroundExercise-induced vasospastic angina (VSA) is a relatively uncommon clinical scenario but may be fatal if not appropriately managed.Case summaryA 56-year-old male patient presented to our hospital for chest oppression on exertion for a 2-week duration. The symptom arose while he was riding a bicycle in the morning but did not arise at rest or on exertion in the afternoon. He was an ex-smoker with a history of hypertension and a family history of sudden death. A resting electrocardiogram (ECG) was normal, and echocardiogram revealed no wall motion abnormalities. Coronary computed tomography angiography indicated a possible stenotic lesion in the circumflex branch. Thus, hospitalization was arranged, and transcatheter coronary angiography (CAG) was performed. In CAG, there was only mild stenosis with small perfusion area in the obtuse marginal branch. A treadmill exercise test was performed the following day to assess the contribution of cardiac ischaemia to his chest symptom on exertion. At 10 metabolic equivalents, he suddenly developed chest pain and prominent ST elevation in leads II, III, aVF, and V2-5 was noted on ECG. The test was immediately terminated, and nitrates were administered. The symptom disappeared, and the patient's ECG normalized, confirming the diagnosis of exercise-induced VSA. Another treadmill exercise test was performed 6 days after vasodilators were started. Even at maximum exercise intensity, neither chest symptoms nor ischaemic changes occurred. The patient was discharged, and the chest symptoms have not returned.DiscussionThis case highlights the importance of appropriate diagnosis and management of exercise-induced VSA.
| S-EPMC6426112 | biostudies-literature
Project description:Despite advances in syncope evaluation strategies and risk stratification, the high cost of syncope is largely driven by extensive and often repetitive testing. This analysis of a large deidentified US claims database compared the use of diagnostic tests, therapeutic procedures, and the recurrence rate of acute syncope events before and after placement of an insertable cardiac monitor (ICM) in syncope patients. The patients had a minimum of 1 year of continuous enrollment before and 2 years after ICM placement. Among 2140 patients identified, a statistically significant reduction in the use of 14 out of 18 tests was observed during follow-up compared with pre-ICM testing. During the 2-year follow-up, 28.3% of patients underwent cardiac therapeutic interventions after a median of 127 days. Significantly fewer patients experienced acute syncope events during the 1st and 2nd years of ICM follow-up compared with the 1-year pre-ICM period, and the frequency of events per patient also decreased. In conclusion, reductions in diagnostic testing and acute syncope events were observed after ICM placement in a large real-world cohort of unexplained syncope patients. Further studies are needed to prospectively assess the impact of ICM vs. short-term monitoring on patient outcomes and healthcare utilization.
| S-EPMC9407126 | biostudies-literature
Project description:We encountered a case of coronary angina refractory to multiple medications, including a calcium channel blocker, nitroglycerin, fasudil (a Rho kinase inhibitor), left stellate ganglion block, thoracic sympathetic ganglion blockade, steroids, and denopamine. During the course of treatment, ventricular tachycardia (VT) occurred due to ST-segment elevation, and an implantable cardioverter-defibrillator was implanted; however, the patient had recurrent VT. A 12‑lead electrocardiogram showed ST elevation localized to leads II, III, and a Vf, and stenting was performed in all main trunks of the right coronary artery. After stenting, the daily angina attacks stopped, VT disappeared, and the chronic phase was controlled with her existing drug therapy, although she had mild chest pain attacks. There is limited evidence regarding the treatment of refractory angina pectoris. In this case, a patient with coronary angina pectoris refractory to various therapies underwent stenting, and the potentially fatal arrhythmia disappeared.Learning objectiveManagement of refractory coronary angina pectoris poses a challenge. Despite attempting conventional therapies, our initial efforts were met with unsuccessful outcomes. Finally, we succeeded in treating the patient with stenting. This case report underscores the challenge of managing refractory coronary angina and explores diverse therapeutic approaches, including conventional medications, sympathetic nerve interventions, and stent placement.
| S-EPMC11523208 | biostudies-literature
Project description:IntroductionPatients with cancer have an increased risk of cardiovascular disease including ischemic heart disease and vice versa. Anticancer drugs and radiotherapy are known to contribute to endothelial injury and vasospasm. However, the relations between vasospastic angina (VSA) and cancer or its treatment are poorly investigated.MethodsA total of 786 patients underwent intracoronary acetylcholine (ACh) provocation tests to diagnose VSA. The positive ACh provocation test was defined as angiographic coronary artery spasm accompanied by chest pain and/or ischemic electrocardiographic changes. Patients were divided into active cancer, a history of cancer, and no cancer according to the status of malignancy. The impact of types of cancer, anticancer drugs, and radiotherapy on VSA was evaluated.ResultsOf 786 patients, 38 (4.8%) and 84 (10.7%) had active cancer and a history of cancer, respectively, and 401 (51.0%) were diagnosed as VSA. There was no significant difference in rates of positive ACh test among patients with active cancer, a history of cancer, and no cancer (39.5% vs. 57.1% vs. 50.9%, p = 0.20). Types of cancer and cancer treatment also had no impact on positive ACh provocation test.ConclusionsIn this cross-sectional observational study, we did not find an association of active and a history of cancer with the diagnosis of VSA. Anticancer treatment including chemotherapy and radiotherapy was not significantly associated with positive ACh provocation test.
| S-EPMC8342335 | biostudies-literature
Project description: Not available
| S-EPMC7424308 | biostudies-literature
Project description: Not available
| S-EPMC5998851 | biostudies-literature
Project description:We herein report a case of a 56-year-old woman with angina pectoris. She visited our emergency room because of chest pain. She finally underwent emergency percutaneous coronary intervention in right coronary artery due to acute coronary syndrome. Several months later, she complained of exertional chest pain again. Exercise-stress electrocardiogram showed ST-segment depression in V2-V6. However, coronary angiography showed no organic stenosis and we conducted acetylcholine provocation test. We finally detected severe coronary artery spasm and diagnosed exercise-induced vasospastic angina (VSA). This case highlights the importance of the recognition of exercise-induced VSA. Exercise-induced VSA needs the definite diagnosis and appropriate treatment. Learning objective Many patients felt chest pain even if they have undergone percutaneous coronary intervention (PCI). This case highlights the importance of the recognition of exercise-induced vasospastic angina (VSA). Exercise-induced VSA needs definite diagnosis and appropriate treatment. This case report describes the importance of precise diagnosis and highlights the recognition of exercise-induced VSA. We recommend the acetylcholine provocation test after PCI in order to determine the diagnosis of exercise-induced VSA.
| S-EPMC8758595 | biostudies-literature
Project description:AimsCoronary microvascular dysfunction and/or vasospasm are potential causes of ischaemia in patients with no obstructive coronary artery disease (INOCA). We tested the hypothesis that these patients also have functional abnormalities in peripheral small arteries.Methods and resultsPatients were prospectively enrolled and categorised as having microvascular angina (MVA), vasospastic angina (VSA) or normal control based on invasive coronary artery function tests incorporating probes of endothelial and endothelial-independent function (acetylcholine and adenosine). Gluteal biopsies of subcutaneous fat were performed in 81 subjects (62 years, 69% female, 59 MVA, 11 VSA, and 11 controls). Resistance arteries were dissected enabling study using wire myography. Maximum relaxation to ACh (endothelial function) was reduced in MVA vs. controls [median 77.6 vs. 98.7%; 95% confidence interval (CI) of difference 2.3-38%; P = 0.0047]. Endothelium-independent relaxation [sodium nitroprusside (SNP)] was similar between all groups. The maximum contractile response to endothelin-1 (ET-1) was greater in MVA (median 121%) vs. controls (100%; 95% CI of median difference 4.7-45%, P = 0.015). Response to the thromboxane agonist, U46619, was also greater in MVA (143%) vs. controls (109%; 95% CI of difference 13-57%, P = 0.003). Patients with VSA had similar abnormal patterns of peripheral vascular reactivity including reduced maximum relaxation to ACh (median 79.0% vs. 98.7%; P = 0.03) and increased response to constrictor agonists including ET-1 (median 125% vs. 100%; P = 0.02). In all groups, resistance arteries were ≈50-fold more sensitive to the constrictor effects of ET-1 compared with U46619.ConclusionsSystemic microvascular abnormalities are common in patients with MVA and VSA. These mechanisms may involve ET-1 and were characterized by endothelial dysfunction and enhanced vasoconstriction.Clinical trial registrationClinicalTrials.gov registration is NCT03193294.
| S-EPMC6284165 | biostudies-literature
Project description:BackgroundSympathetic overactivity has been linked to vasospastic angina (VSA), although the exact pathophysiology of VSA is poorly understood. The purpose of this study is to assess if renal sympathetic denervation (RDN) reduces cardiac sympathetic nerve activity with a subsequent beneficial effect on angina relief in patients with refractory VSA.Methods and resultsCardiac sympathetic nerve activity was assessed prior to procedure and at 6 months post-procedure using iodine-123 labeled meta-iodobenzylguanidine (123I-MIBG) imaging. The Seattle Angina questionnaire (SAQ) was used to assess the degree to which the disease impacts quality of life. No significant change was observed in early HMR (pre-RDN: 2.74 [2.10 to 3.21] vs 6 months post-RDN: 2.57 [2.20 to 3.00]; P = 0.76), and late HMR (pre-RDN: 2.56 [2.18 to 3.20] vs 6 months post-RDN: 2.36 [2.13 to 3.22]; P = 0.22). Additionally, no change was seen in WR (P = 0.22). SAQ results revealed significant improvements in perceived physical limitation, angina frequency, and quality of life at 6 months (P < 0.05 for all).ConclusionRDN resulted in improvements in angina class and quality of life at 6 months in patients with refractory VSA. RDN, however, did not result in significant changes in cardiac sympathetic nerve activity as measured using 123I-MIBG. The latter observation should be considered with caution given the small sample size of this study. Larger studies are needed to assess this further.
| S-EPMC7749092 | biostudies-literature
Project description:A 46-year-old male presented with acute chest pain, monomorphic ventricular tachycardia, and non-ST-segment elevation myocardial infarction. He was found to have myocardial bridging of the mid left anterior descending coronary artery on coronary angiography and mildly reduced left ventricular ejection fraction with anteroseptal and apical hypokinesia. The patient was treated with antiplatelet therapy, guideline-directed medical therapy for heart failure, and had improvement in symptoms and left ventricular function 1 month later. The case highlights the complex way myocardial bridging may present and its potential to cause major adverse cardiovascular events.
| S-EPMC11861925 | biostudies-literature