Holter ECG diagnosis of nicotine-spray induced ventricular fibrillation. An unusual case of Prinzmetal variant angina.

We report on an interesting case of resuscitated sudden cardiac death (SDC) in a 51-year-old with hypertension and positive family history for SDC. The patient was resuscitated and an emergency angiogram ruled out coronary artery disease. Cardio-MRT ruled structural disease or infection. Holter and telemetry monitoring revealed premature ventricular complexes and transient ST-changes followed by anginaepisodes in correlation with the use of the nicotine-replacement-spray. The patient was urged to quit smoking and smoking-substitutes. Medical therapy with calcium-channelblocker and a long acting nitrate was administered. One-month follow up reported no arrhythmic or angina events.

[Many possible causes of variant angina]. / Veel mogelijke oorzaken voor vasospastische angina pectoris.

BACKGROUND: Variant angina, or vasospastic angina, is a form of angina caused by vasospasm of the coronary arteries, probably caused by endothelial dysfunction. This form of angina is provoked by non-classical risk factors such as stress, alcohol use, use of sympathomimetics and low environmental temperatures, but also by smoking. Treatment is based on elimination of risk factors and vasodilator therapy with nitrates and long-acting calcium antagonists. CASE DESCRIPTION: We present a 68-year-old woman with recurring thoracalgia at rest and during exercise, suggestive of severe variant angina in more than one coronary artery. Despite elimination of risk factors and administration of vasodilatory therapy the treatment was initially insufficient. It eventually emerged that the probable cause was frequent use of a vasoconstrictive nasal spray, although this was not described in literature, and not originally mentioned by the patient. CONCLUSION: A thorough case history is of vital importance in a patient presenting with a history suggestive of variant angina. Even undescribed and apparently less important risk factors can be responsible for persistence of symptoms, and can lead to an applied treatment not producing the desired result.

Variant angina in moyamoya disease--a correlative etiology and different presentation: a case report.

INTRODUCTION: Moyamoya disease is characterized by progressive steno-occlusive changes of the distal internal carotid and developed collateral vasculature, so called 'moyamoya' vessels at the base of the brain. Variant angina is a rare occurrence in patients with moyamoya disease. CASE PRESENTATION: Here we report the case of a 41-year-old Korean woman who developed chest pain after indirect revascularization surgery of moyamoya disease. A treadmill test and an exercise stress echocardiograph showed positive results, but there was no significant major coronary arteries stenosis. Suspicious of vasospasm, we conducted an ergonovine spasm stimulation test, which demonstrated tight stenosis of her proximal left anterior descending artery. At the site of spasm, intravascular ultrasound virtual histology showed intraluminal fibrous plaque. CONCLUSION: Physicians who follow up patients with moyamoya disease would need to be aware of the possibility of cardiac ischemia as well as neurological manifestations.

K2--not the spice of life; synthetic cannabinoids and ST elevation myocardial infarction: a case report.

INTRODUCTION: The adverse effects of synthetic cannabinoids are not well-described nor have they been thoroughly studied. CASE REPORT: A 16-year-old male with a past medical history of asthma and attention deficit hyperactivity disorder (ADHD) presented to the emergency department (ED) complaining of 24 h of substernal pressure associated with dyspnea, nausea, and vomiting. He reported smoking tobacco cigarettes daily and occasional marijuana use but denied recent use of marijuana. The initial electrocardiogram (EKG) revealed ST-segment elevations in leads II, III, AVF, and V4-V6. The initial troponin level was reported as 1.47 ng/mL, and the initial creatine kinase MB (CKMB) level was 17.5 ng/mL. The patient admitted to smoking "K2" 60-90 min prior to the onset of symptoms. The patient manifested persistent ST elevations with a peak troponin of 8.29 ng/mL. The urine drug immunoassay was positive for benzodiazepines and opiates. Cardiac catheterization revealed normal coronary arteries, no wall motion abnormalities, and normal systolic function. DISCUSSION: Synthetic cannabinoids may have significant potential adverse effects. Chest pain due to myocardial ischemia is rare in adolescents. When evaluating patients with chest pain, it is important to elicit a detailed drug history, specifically inquiring about synthetic cannabinoid use. Urine drug immunoassays may be unreliable and in this case did not detect synthetic cannabinoids.

A rare cause of cardiogenic shock: variant angina.

Variant angina (VA) is a clinical syndrome caused by spontaneous vasospasm of the epicardial coronary artery which is characterized by episodes of angina. Endothelial dysfunction and neurohormonal hyperactivity are important factors in pathogenesis of VA. Although patient prognosis is good, VA may be one of the reasons of sudden cardiac death (SCD) in case of persistent ST segment elevation and malignant arrhythmias. Therefore, early treatment of VA is crucial for prevention of malignant arrhythmias and SCD. In this case report we describe a case of VA presented with cardiogenic shock and malignant ventricular arrhythmia.

Elevated troponin levels in previously healthy children: value of diagnostic modalities and the importance of a drug screen.

BACKGROUND: Myocardial injury in previously healthy children is rare, with a wide range of aetiologies. It is increasingly being identified on the basis of elevated troponin levels during routine evaluation of cardiorespiratory symptoms. Establishing the aetiology remains challenging because of the lack of an accepted work-up algorithm. Our objective was to delineate the contribution of diagnostic modalities and troponin patterns towards the final diagnosis. METHODS: A retrospective chart review of previously healthy patients admitted to the Pediatric Cardiology Service with myocardial injury was carried out. Data analysed included echocardiograms, electrocardiograms, cardiac catheterisations, magnetic resonance imaging, drug screen tests, troponin values, and final diagnosis. RESULTS: A total of 32 patients were identified. The diagnoses were: myocarditis in 16 patients, vasospasm due to drug use in seven, myopericarditis in six, anomalous coronary artery origins in two, and Prinzmetal's angina in one patient. The electrocardiograms were abnormal in 27 of the 32 patients (84%), echocardiograms in 18 of the 32 patients (56%), cardiac magnetic resonance imaging in two of the four patients (50%), urine drug screen in five of the 25 patients (20%), and cardiac catheterisations in two of the 15 patients (13%). CONCLUSIONS: Myocarditis is the most common aetiology of myocardial injury in children. Clinical history remains the basic screening tool; drug screens help identify coronary vasospasms secondary to drug use (22% of our cohort). Patients with anomalous coronaries had exertional symptoms. Initial troponin levels and progression were not diagnostic or prognostic. Catheterisation is of limited value and did not change management. Magnetic resonance imaging with gadolinium enhancement is probably the most useful test when initial evaluation is not diagnostic.

[One patient - many faces of myocardial ischaemia]. / Jedna pacjentka - rózne oblicza choroby niedokrwiennej serca.

We present the case of a woman treated with coronary angioplasty due to non-ST segment elevation myocardial infarction,then again because of restenosis, who continued to complain of chest pain and syncope. Holter electrocardiogram recording revealed atrioventricular block related to ST-segment elevations and variant angina was diagnosed. Despite administered medications, the patient required pacemaker implantation.

Cardiopulmonary arrest caused by coronary spasm after coronary vasodilator withdrawal during the peri-operative period of gastrectomy.

Calcium antagonists, nicorandil and long-acting nitrates are highly effective for preventing coronary spasm. The withdrawal of coronary vasodilators, especially calcium antagonists, is risky in cases of vasospastic angina. We herein present a case of cardiopulmonary arrest that occurred due to coronary spasm triggered by the discontinuation of coronary vasodilators during the peri-operative period of gastrectomy. Vasospastic angina patients who are not able to take oral coronary vasodilators in the peri-operative period should be maintained on a parenteral vasodilator until they are able to take them orally. Physicians should also be aware of the possible development of nitrate tolerance in patients on prolonged nitrate therapy.

Eosinophilic coronary periarteritis (vasospastic angina and sudden death), a new type of coronary arteritis: report of seven autopsy cases and a review of the literature.

A previously reported autopsy case of eosinophilic coronary periarteritis (ECPA, or isolated eosinophilic coronary periarteritis, IECPA), and an additional six autopsy cases of ECPA are reported. In addition, another four autopsy cases of ECPA reported in the literature are discussed. Fifteen cases of ECPA with spontaneous coronary dissection (hematoma), which appeared in the literature from 1987 to 2011, are also reviewed. The characteristic clinico-pathological findings of ECPA are: (a) variant angina (Prinzmetal's vasospastic angina) appeared mainly from evening to early in the morning; (b) allergy or allergic history could be identified in only three of a total of 11 cases; (c) sudden unexpected death (sudden cardiac death) usually occurred early in the morning; (d) eosinophilic inflammation limited to the adventitia and periadventitial soft issue appeared in the epicardial large coronary arteries, chiefly in the left coronary anterior descending artery; (e) fibrinoid necrosis or granuloma could not be found in or around the inflammatory area; (f) no type of vasculitis could be found in any other tissues or organs (i.e., localized and non-systemic periarteritis); (g) ECPA was frequently accompanied by spontaneous coronary arterial dissection (SCAD) in the affected wall; and (h) ECPA without SCAD appeared mainly in men (male/female ratio was 8:3), while EPCA with SCAD appeared in almost all female cases (male/female ratio was 1:14). Although the etiology and pathogenesis are still unknown, we believe that ECPA (with or without SCAD) might be a distinct new type of coronary arteritis.

Persistent angina pectoris, cardiac mortality and myocardial infarction during a 12 year follow-up in 273 variant angina patients without significant fixed coronary stenosis.

The incidence of cardiac events in patients with variant angina pectoris without significant coronary stenosis and ST-segment elevation was analyzed during a 12-year follow-up period in 273 consecutive patients (82% men) admitted from 1986 through 2010. Among the 252 patients who underwent electrocardiography during pain, 205 had ST-segment elevation (82%) and 45 had ST-segment depression (18%). During index hospitalization, angina occurred in 179 patients (66%), ventricular tachycardia or fibrillation in 28 (10%), and complete atrioventricular block in 3 (1%), but there were no deaths or myocardial infarctions (MIs). At 140 months, angina was still present in 129 patients (47%), but frequent angina (>10 episodes/year) occurred in only 6%. Total mortality, cardiac mortality, and MI rates were 24%, 7.0%, and 6%, respectively. Cardiac death or MI occurred in 28 patients (10%), associated with tobacco smoking (p = 0.004), antecedent "first-wind" angina (p = 0.020), and angina during hospitalization (p = 0.044) and with continued smoking (p = 0.056) and recurrent angina during follow-up (p <0.001). Multivariate analysis identified age (p = 0.001), antecedent infarction (p = 0.005), first-wind angina (p = 0.009), and smoking at index hospitalization (p = 0.027) as predictors of total mortality and treatment with calcium antagonists (p = 0.047) and smoking during follow-up (p = 0.110) for cardiac mortality and MI. In conclusion, during 12-year follow-up, patients with variant angina pectoris, mostly with ST-segment elevation during pain, had a reduced incidence of cardiac mortality and MI, associated with first-wind angina, persistent angina, and continued smoking.

Vasospastic angina with J-wave pattern and polymorphic ventricular tachycardia effectively treated with quinidine.

BACKGROUND: Myocardial ischemia during coronary spasm may generate malignant ventricular arrhythmias. The J-wave pattern was suggested to be a marker of a disorder associated with life-threatening arrhythmias. RESULTS: We report the case of a patient with vasospastic angina and J-wave pattern in inferior and lateral leads associated with polymorphic ventricular tachycardia which was effectively treated only with quinidine-vasodilating drugs were not able to prevent the arrhythmia although they were effective in preventing ischemic events. CONCLUSION: The J-wave pattern in inferolateral leads may be a sign of electrical vulnerability to lethal ventricular arrhythmia in patients suffering from vasospastic angina--quinidine can effectively prevent such arrhythmias in these patients.

Clinical implications of an implantable cardioverter-defibrillator in patients with vasospastic angina and lethal ventricular arrhythmia.

OBJECTIVES: The present study was performed to investigate the clinical implications of an implantable cardioverter-defibrillator (ICD) in patients with vasospastic angina (VSA) resuscitated from lethal ventricular arrhythmia. BACKGROUND: The prognosis of VSA is known to be good with medication; however, ventricular arrhythmia and cardiopulmonary arrest are rare but life-threatening complications of this disease. The ICD is a proven modality for patients with ventricular arrhythmia, but the clinical implications in this population remain to be elucidated. METHODS: We conducted a retrospective, observational, multicenter study involving patients with an ICD due to documented ventricular arrhythmia and VSA diagnosed by acetylcholine provocation test. All patients were followed up for appropriate ICD therapy, sudden cardiac arrest, or death from all causes. RESULTS: Twenty-three patients were included in the present study and completely followed up. All patients are still alive. During a follow-up of 2.9 years (median 2.1 years), 4 ventricular fibrillations and 1 episode of pulseless electrical activity occurred in 5 patients (21.7%). There were no statistically significant differences in patient characteristics between the recurrence and nonrecurrence groups, including medication, smoking status, and whether the patient was or was not free of symptoms after ICD implantation. CONCLUSIONS: Patients with VSA and lethal ventricular arrhythmia are a population at high risk for recurrence of cardiopulmonary arrest, and there is no reliable indicator for predicting recurrence of ventricular arrhythmia. Insertion of an ICD with medication for VSA is appropriate for this high-risk population.

Differential local spasticity in myocardial bridges.

To illustrate the effect of myocardial bridges on coronary vascular tone, we describe the cases of 2 patients with different clinical presentations in the context of reproducible increased spasticity at the site of myocardial bridging. One had an episode of takotsubo cardiomyopathy, and one developed typical Prinzmetal angina while receiving desmopressin treatment for pituitary insufficiency. In both patients, acetylcholine challenge clearly revealed both the presence and the severity of myocardial bridging while producing several recognizable degrees of abnormal spastic tendency.Both baseline functional states and responses to different medications correlate with spastic tendency and enable the characterization of individual cases. Understanding the spectrum of spastic conditions might help to clarify the causes of atypical ischemic events, especially in patients with myocardial bridging.

A Becker myotonia patient with compound heterozygosity for CLCN1 mutations and Prinzmetal angina pectoris.

Becker myotonia is a recessive muscle disease with prevalence of > 1:50,000. It is caused by markedly reduced function of the chloride channel encoded by CLCN1. We describe a Polish patient with severe myotonia, transient weakness, and muscle cramps who only responds to lidocaine. In addition, the patient has Prinzmetal angina pectoris and multiple lipomatosis. He is compound heterozygeous for a novel p.W303X and a frequent p.R894X CLCN1 mutation. CLCN1 exon number variation was excluded by MLPA. His son with latent myotonia was heterozygeous for p.R894X. We discuss the potential relations of the three rare diseases and the inheritance of p.R894X.

Prinzmetal's angina in a patient with angiosarcoma of the right cardiac chambers.

Variant (Prinzmetal's) angina pectoris is a clinical syndrome characterized by the presence of angina at rest, coinciding with a transient ST-segment elevation. This syndrome is often caused by vasospasm, either on a normal coronary artery or at the site of a coronary atherosclerotic stenosis. We describe a classic case of variant angina associated with an angiosarcoma of the right heart chambers.

Kounis syndrome in a patient with ovarian cancer and allergy to iodinated contrast media: report of a case of vasospastic angina induced by chemotherapy.

We report the case of a 71-year-old woman with previous coronary angioplasty, ovarian cancer with multiple metastases and allergy to iodinated contrast media, who developed vasospastic angina after several treatments with cisplatin and cyclophosphamide, so that we considered this as a case of "allergic angina" or Kounis syndrome (type II variant). The patient underwent standard anti-ischemic therapy with nitrates, calcium blocking agents and enoxaparin so having an uneventful outcome.