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Objectives We conducted a randomised, double blind, placebo controlled trial to assess the efficacy and safety of cilostazol, a selective inhibitor of phosphodiesterase 3, in patients with vasospastic angina (VSA). Background Cilostazol has been shown to induce vascular dilatation, but its efficacy in patients with VSA is unknown. Methods Between October 2011 and July 2012, 50 patients with confirmed VSA who had ≥1 angina episodes/week despite amlodipine therapy (5 mg/day) were randomly assigned to receive either cilostazol (up to 200 mg/day) or placebo for 4 weeks. All patients were given diaries to record the frequency and severity of chest pain (0–10 grading). The primary endpoint was the relative reduction of the weekly incidence of chest pain. Results Baseline characteristics were similar between the two groups. Among 49 evaluable patients (25 in the cilostazol group, 24 in the placebo group), the primary endpoint was significantly greater in the cilostazol group compared with the placebo group (−66.5±88.6% vs −17.6±140.1%, respectively, p=0.009). The secondary endpoints, including a change in the frequency of chest pain (−3.7±0.5 vs −1.9±0.6, respectively, p=0.029), a change in the chest pain severity scale (−2.8±0.4 vs −1.1±0.4, respectively, p=0.003), and the proportion of chest pain-free patients (76.0% vs 33.3%, respectively, p=0.003) also significantly favoured cilostazol. Headache was the most common adverse event in both groups (40.0% vs 20.8%, respectively, p=0.217). Conclusions Cilostazol is an effective therapy for patients with VSA uncontrolled by conventional amlodipine therapy, and has no serious side effects. Trial registration number NCT01444885.

Background Vasospastic angina (VSA) is characterized by coronary spasm, which can be aggravated by vasoactive substances such as serotonin. Hypothesis Sarpogrelate, a selective serotonin receptor antagonist, and high‐dose statin have some effects on the reduction of coronary spasm in patients with VSA. Methods We recruited 100 patients with angiographically confirmed VSA, and randomly assigned them into four groups: sarpogrelate with high‐dose statin (Group A, n = 25), sarpogrelate with low‐dose or no statin (Group B, n = 25), placebo with high‐dose statin (Group C, n = 25), and placebo with low‐dose or no statin (Group D, n = 25). The primary endpoint was the remission of coronary spasm on 1‐year follow‐up provocation test. Results The most common site of coronary spasm was left anterior descending artery (42%). Most patients (96%) took calcium channel blockers, and 46% were treated with vasodilators. Overall, 40% of patients reported no chest pain at 1 year, and 23% showed complete remission of coronary spasm on 1‐year follow‐up provocation test. No difference was observed in symptomatic and angiographically complete remission rate between the sarpogrelate and the placebo group. Although the apolipoprotein B level at the 1‐year follow‐up was significantly lower in the high‐dose statin group, symptomatic and angiographic outcomes were not different according to statin intensity. Distal thrombolysis in myocardial infarction (TIMI) flow on initial provocation test was independently associated with angiographically complete remission. Conclusions Sarpogrelate or high‐dose statin did not significantly improve the angiographic remission rate in patients with VSA. Distal TIMI flow on initial provocation test could predict the complete remission of coronary spasm at follow‐up.

Vasospastic angina is a well-established cause of chest pain that is caused by coronary artery spasm. It can be clinically diagnosed during a spontaneous episode by documenting nitrate-responsive rest angina with associated transient ischaemic ECG changes but more often requires provocative coronary spasm testing with acetylcholine during coronary angiography. Vasospastic angina may result in recurrent episodes of angina (including nocturnal angina), which can progress on to major adverse cardiac events. Calcium channel blockers are first-line therapy for this condition, given their anti-anginal and cardioprotective benefits. Despite an established diagnostic and therapeutic management pathway for vasospastic angina, this diagnosis is often overlooked in patients presenting with chest pain. Thus, there is need for increased clinical awareness of vasospastic angina to improve outcomes in affected patients.

Although heart failure (HF) is a clinical syndrome that becomes worse over time, certain cases can be reversed with appropriate treatments. While coronary artery spasm (CAS) is still underappreciated and may be misdiagnosed, ischemia due to coronary artery disease and CAS is becoming the single most frequent cause of HF worldwide. CAS could lead to syncope, HF, arrhythmias, and myocardial ischemic syndromes such as asymptomatic ischemia, rest and/or effort angina, myocardial infarction, and sudden death. Albeit the clinical significance of asymptomatic CAS has been undervalued, affected individuals compared with those with classic Heberden’s angina pectoris are at higher risk of syncope, life-threatening arrhythmias, and sudden death. As a result, a prompt diagnosis implements appropriate treatment strategies, which have significant life-changing consequences to prevent CAS-related complications, such as HF. Although an accurate diagnosis depends mainly on coronary angiography and provocative testing, clinical characteristics may help decision-making. Because the majority of CAS-related HF (CASHF) patients present with less severe phenotypes than overt HF, it underscores the importance of understanding risk factors correlated with CAS to prevent the future burden of HF. This narrative literature review summarises and discusses separately the epidemiology, clinical features, pathophysiology, and management of patients with CASHF.

BackgroundThe concept of non-atherosclerotic coronary artery pathology in sudden cardiac death (SCD) has not been given the attention it deserves.ObjectiveTo determine the incidence of non-atherosclerotic coronary artery pathology in SCD and raise awareness among cardiologists and pathologists alike.DesignRetrospective non-case-controlled analysis.SettingCardiac pathology centre at the National Heart and Lung Institute and Royal Brompton Hospital.SubjectsBetween 1994 and 2008, the hearts of 1647 people undergoing SCD were referred for pathological assessment to ascertain the precise aetiology of SCD.ResultsFifty (3.0%) of the 1647 cases of SCD were associated with non-atherosclerotic coronary pathology (31 male subjects (62%) and 19 female subjects (38%, age range (8 weeks–71 years)). Twenty four of the 50 cases had anomalous coronary arteries (48%); eight cases had coronary artery dissection (16%); six cases had coronary artery vasculitis (12%); six cases had coronary artery spasm (12%); three cases had idiopathic arterial calcification of infancy (6%); two cases had fibromuscular dysplasia (4%) and one case had a benign tumour occluding the left coronary ostium (2%). Only 20 of the 50 patients (40%) were documented to have experienced cardiac symptoms such as syncope, chest pain on exertion or breathlessness before their SCD. Twelve of the patients (24%) died during or immediately after physical exertion.ConclusionNon-atherosclerotic coronary disease is associated with sudden death in all age groups, particularly younger, male patients. Cardiologists need to be aware of these entities and investigate any patient who has cardiac symptoms especially with exertion.

Background An early repolarization (ER) pattern is a risk factor for ventricular fibrillation (VF) in patients with vasospastic angina (VSA) caused by a coronary artery spasm. However, its detailed characteristics and prognostic value for VF remain unclear. Thus, we investigated the relationship between ER and VF in patients with VSA. Hypothesis The ER pattern is associated with VF in patients with VSA. Methods In this systematic review and meta‐analysis, we searched PubMed, Embase, Cochrane Library, and Web of Science databases for eligible studies published between January 2011 and December 2020; 8 studies with 1761 patients were included in the final analysis. Results The ER pattern significantly predicted adverse cardiovascular events (ACEs) and VF (odds ratio [OR] = 5.13, 95% confidence interval [95% CI]: 3.16–8.35, p < .00001 and OR = 5.20, 95% CI: 3.05–8.87, p < .00001). The presence of ER in the inferior leads increased the VF risk (OR = 7.80, 95% CI: 4.04–15.05, p < .00001), regardless of the J‐point morphology or type of ST‐segment elevation in the ER pattern. A horizontal/descending ST‐segment elevation was significantly associated with VF in patients with or without an ER pattern during a coronary spasm (OR = 2.28, 95% CI: 1.07–4.88, p = .03). However, obstructive coronary artery disease was unrelated to the ER pattern (OR = 0.82, 95% CI: 0.27–2.53, p = .73). Conclusions An ER pattern is significantly associated with an increased risk of ACE in patients with VSA. An inferior ER pattern with horizontal/descending ST‐segment elevation confers the highest risk for VF during VSA onset. Nevertheless, the ER pattern is not associated with obstructive coronary artery disease.

Coronary artery spasms (CAS) can manifest in various forms, from silent ischemia to severe cardiac events like myocardial infarction and sudden death. This case involves a 56‐year‐old male with recurrent ischemic chest pain and varying ECG signs. Cardiac catheterization revealed multiple coronary spasms that resolved spontaneously or with intracoronary nitroglycerin. The report emphasizes the severe presentations of multiple CAS and the importance of thorough diagnostic evaluation to avoid unnecessary interventions, highlighting the diagnostic challenges in managing such cases. This case report highlights the severe presentations and diagnostic challenges associated with simultaneous spasms in multiple coronary arteries, emphasizing the need for comprehensive evaluation and appropriate management to prevent unnecessary interventions and improve patient outcomes.

Background Myocarditis refers to the inflammation of the myocardium caused by infection or autoimmune disease that may or may not present with clinical manifestations, such as gastrointestinal symptoms, dyspnea, chest pain, or sudden death. Although myocarditis and coronary artery vasospasm may mimic ST-segment elevation myocardial infarction (STEMI) with normal coronary arteries on angiography, acute myocarditis rarely causes coronary artery spasm. Here, we report a case of coronary artery spasm with reversible electrocardiographic changes mimicking STEMI in an adolescent with acute myocarditis. Case presentation A 15-year-old boy present with sudden-onset repeated chest pain following a 3-day history of flu-like illness. Cardiac biomarkers were significantly elevated. Electrocardiography showed ST-segment elevation in the absence of detectable vasospasm on coronary angiography. These findings were consistent with the diagnosis of coronary artery spasm secondary to acute myocarditis. Treatment with immunoglobulin for 2 days improved his condition. The patient was discharged on the 12th day with complete resolution of symptoms and normalization of electrocardiogram findings. Conclusions We reported a case of coronary artery spasm due to acute myocarditis. This study highlights the importance of considering coronary artery spasm due to acute myocarditis as a differential diagnosis in patients presenting with signs of STEMI as these diseases have different medical management strategies.

The study compared the 2-year outcomes of patients diagnosed with acute myocardial infarction (AMI) triggered by coronary artery atherosclerosis and AMI caused by coronary artery spasm. A total of 36,797 patients in the Korea AMI Registry were grouped into 2 categories—(1) AMI due to coronary artery spasm without stenotic lesion (CAS-AMI, n = 484); and (2) AMI induced by coronary artery atherosclerosis (CAA-AMI, n = 36,313). The major clinical outcomes of the 2 groups were compared over a 2-year clinical follow-up period. Major adverse cardiac events (MACE) were defined as the composite of total death, nonfatal myocardial infarction, and repeat revascularization. The incidence of MACE (7.1% vs 11.1%; p = 0.007) and repeat revascularization (0.4% vs 4.2%; p <0.001) in the CAS-AMI group were significantly lower than in the CAA-AMI group at 2 years. However, the incidence of total death and nonfatal myocardial infarction was similar in both the groups. Aborted cardiac arrest was strongly associated with 2-year mortality in the CAS-AMI group (hazard ratios 13.5, 95% confidence interval 5.34 to 34.15, p <0.001) The incidence of MACE in CAS-AMI patients was significantly lower than in the CAA-AMI group of patients up to 2 years due to the relatively lower rate of repeat revascularization in CAS-AMI patients. However, the incidence of total death or nonfatal myocardial infarction in CAS-AMI patients was not different from that of patients with CAA-AMI.

BackgroundInflammation, oxidative stress (OS), atherosclerosis and resistant hypertension (RH) are common features of chronic kidney disease (CKD) leading to a higher risk of death from cardiovascular disease. These effects seem to be modulated by impaired anti-oxidant, anti-inflammatory and reverse cholesterol transport actions of high-density lipoprotein cholesterol (HDL). HDL prevents and reverses monocyte recruitment and activation into the arterial wall and impairs endothelial adhesion molecule expression. Recently, monocyte count to HDL-cholesterol ratio (MHR) has emerged as a potential marker of inflammation and OS, demonstrating to be relevant in CKD. Our research was aimed to assess, for the first time, its reliability in RH.MethodsWe performed a retrospective study on 214 patients with CKD and arterial hypertension who were admitted between January and June 2019 to our Department, 72 of whom were diagnosed with RH.ResultsMHR appeared inversely related to eGFR (ρ = − 0.163; P = 0.0172). MHR was significantly higher among RH patients compared to non-RH ones (12.39 [IQR 10.67–16.05] versus 7.30 [5.49–9.06]; P < 0.0001). Moreover, MHR was significantly different according to the number of anti-hypertensive drugs per patient in the whole study cohort (F = 46.723; P < 0.001) as well as in the non-RH group (F = 14.191; P < 0.001). Moreover, MHR positively correlates with diabetes mellitus (ρ = 0.253; P = 0.0002), white blood cells (ρ = 0.664; P < 0.0001) and C-reactive protein (ρ = 0.563; P < 0.0001).ConclusionsMHR may be a reliable biomarker due to the connection between HDL and monocytes. Our study suggests that MHR is linked with the use of multiple anti-hypertensive therapy and resistant hypertension in CKD patients, and can be a useful ratio to implement appropriate treatment strategies.