ST-segment elevation and the Tpeak-Tend/QT ratio predict the occurrence of malignant arrhythmia events in patients with vasospastic angina.

BACKGROUND: ST-segment elevation (STE) and an increased Tpeak-Tend interval (Tp-e) have prognostic value for malignant arrhythmia events (MAEs) in patients with ST-segment elevation myocardial infarction (STEMI) and Brugada syndrome. Whether STE could predict MAEs and has an electrophysiological relationship with Tp-e in electrocardiogram (ECG) of vasospastic angina (VA) patients needs to be elucidated. METHODS: Sixty-five patients with VA and 23 patients with VA complicated by MAEs were enrolled. The relationship of ECG parameters and MAEs (defined as ventricular tachycardia/ventricular fibrillation (VT/VF), syncope, and aborted sudden death) was analyzed by t-test, regression and receiver operating characteristic (ROC) curve analyses. RESULTS: Patients with MAEs showed greater STE (P<0.001) and corrected QT dispersion (cQTd) (P=0.021), a longer corrected Tp-e interval (cTp-e) (P<0.001), and a larger Tp-e/QT ratio (P<0.001) than those in non-MAE groups. Univariate analysis revealed that cQTd (odds ratio (OR)=1.065; P=0.020), cTp-e (OR=1.159; P=0.001), Tp-e/QT (OR=1.344, P=0.002), and STE (OR=5.655, P<0.001) were significantly associated with MAEs. In the multivariate analysis, Tp-e/QT and STE remained predictors of MAEs. ROC curve analysis showed that the areas under curve (AUCs) for Tp-e/QT (AUC=0.944) and STE (AUC=0.974) were not significantly different (P>0.05), but both were significantly different than AUCs for cQTd (AUC=0.724) and cTp-e (AUC=0.841) (all P<0.05). STE was well fitted with the Tp-e/QT ratio in a multivariable linear regression model. CONCLUSIONS: STE and increased Tp-e/QT ratio had related electrophysiological properties and were independent prognostic indicators of MAEs in patients with VA.

Early repolarization is involved in ventricular fibrillation in patients with variant angina.

BACKGROUND: Variant angina (VA) is caused by reversible coronary artery spasm, which is characterized by chest pain with ST segment elevations on a standard 12-lead electrocardiogram (ECG) at rest. VA attack often causes lethal ventricular arrhythmia. The early repolarization (ER) pattern is associated with ventricular fibrillation (VF). However, whether the ER pattern is involved in VF in patients with VA is not known. We investigated the association between the ER pattern and VF in patients with VA. METHODS: Fifty patients underwent induction of ST elevation on 12-lead ECGs with total or nearly total occlusion by provocation test (VA patients). Twelve of these patients underwent induction of VF or had documented VF before hospital admission (VF occurrence group). The J-wave morphology was characterized as exhibiting notching or slurring. The amplitude of each J wave was measured manually with amplified waveforms. RESULTS: ER patterns were observed significantly more often in the VF occurrence group than in the non-VF occurrence group (P = 0.007). The J-wave amplitude was significantly higher in the VF occurrence group compared with the non-VF occurrence group (P = 0.02). Univariate analyses suggested that age, smoking, and ER patterns were associated with VF. Upon multivariate analyses, age (odds ratio [OR] = 0.880; 95% confidence interval [CI]: 0.794-0.975; P = 0.014) and ER patterns (OR = 8.937; 95% CI:1.661-48.06; P = 0.011) predicted VF independently. CONCLUSIONS: These data suggest that an ER pattern in VA patients is a risk factor for VF. The ER pattern may be one of the useful factors for adaptation of implantation of implantable cardioverter-defibrillator in patients with coronary spasm-induced VF.

Vasospastic Angina Presenting With Syncope and Chest Pain: A Case Report and Brief Literature Review.

A 65-year-old male presented to the hospital with chest pain associated with recurrent syncope. He had a history of coronary artery disease and a long-standing history of smoking. While he was hospitalized, he had an episode of chest pain during which he was found to have transient ST segment elevation in the inferior leads. He was also noted to have a brief cardiac tachyarrhythmia. Coronary arteriography revealed vasospasm of the left anterior descending artery and right coronary artery, which were relieved to a significant extent after administration of intracoronary nitroglycerin. Subsequent angiograms and fractional flow reserve studies, demonstrated underlying non-obstructive coronary artery disease at the sites of spasm. No percutaneous coronary intervention was pursued. The patient was started on a calcium channel blocker on dismissal from the hospital. Upon follow up several months later, he remained free of symptoms that brought him to the hospital.

The Usefulness of Spinal Cord Stimulation for Chronic Pain Due to Combined Vasospastic Prinzmetal Angina and Diabetic Neuropathic Pain of the Lower Limbs.

OBJECTIVE: To describe an unusual case of combined neuropathic and ischemia-induced chronic pain in a patient who was treated with one high thoracic paddle lead. BACKGROUND: To the best of our knowledge, the use of spinal cord stimulation (SCS) utilizing a single lead as a treatment strategy for combined Prinzmetal angina, a cardiac ischemia-induced disturbance of nociceptive perception, and diabetic neuropathy of the lower limbs has rarely been described. CASE REPORT: The underlying pain conditions and SCS technique used to treat both types of pain-Prinzmetal angina and lower-limb diabetic neuropathy-in a 73-year-old patient experiencing medical or interventional refractory complex pain syndrome are described. The SCS electrode was placed in the anatomical midline with a T2- to T3-level laminotomy and externalized for postoperative trial stimulation with systemic antibiotic administration. RESULTS: After 8 months, stable pain control was achieved. No complications occurred. CONCLUSION: We present a chronic pain syndrome due to combined Prinzmetal angina and diabetic neuropathy of the lower limbs with sustained pain relief utilizing a single SCS lead.

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.

[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.

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.

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.

[Tolerance and efficacy of early nicotine substitution after acute coronary syndromes]. / Tolérance et efficacité de la substitution nicotinique précoce au décours d'un syndrome coronaire aigu.

The object of this study was to assess the cardiovascular tolerance and efficacy of early nicotine substitution therapy in 100 patients admitted to the Coronary Care Unit for acute coronary syndromes (ACS). The files of the first 100 consecutive patients having received nicotine substitution therapy immediately after an ACS were consulted retrospectively and a questionnaire was sent to all patients. A reply was obtained in 90% of cases. In this series, there was a 7% rate of cardiovascular events in the days following hospital discharge, comparable to previously reported results. The smoking relapse rate at six months after the ACS was 38.9%, a percentage which was less than in previously reported series. Although consultations to help stop smoking and nicotine substitution did not seem to have significant benefits in this study, the authors recommend continuing and improving the management of coronary patients who smoke.

[Malignant arrhythmia in a patient with variant (Prinzmetal's) angina pectoris]. / Maligní arytmie u pacienta s variantní (Prinzmetalovou) anginou pectoris.

Malignant arrhythmia is a frequent complication of myocardial ischemia due to the occurrence of coronary artery spasm. The paper describes a patient with variant angina pectoris with an ICD implant who was repeatedly resuscitated for circulatory arrest in malignant arrhythmia. During myocardial ischemia the ECG showed elevations in the ST segments in the region of the ventral cardiac wall, with the formation of permanent polymorphous chamber tachycardia. External defibrillation was necessary due to recurrent tachyarrhythmias. A spasm developed when the RIA (radio immuno assay) was introduced during coronarography. The spasm started in the periphery of the artery and extended as far as the area of bifurcation with RD, with transitory closure of the artery and the development of chamber tachycardia. The patient fully recovered after the addition of Ca-blocker, nitrate depot and the withdrawal of the beta-blocker.

Anginalike pain and normal coronary arteries. Uncovering cardiac syndromes that mimic CAD.

Atherosclerotic CAD is the most common cause of cardiac chest pain in Western countries. Other cardiac syndromes may also cause anginalike pain and may be difficult to differentiate from atherosclerotic CAD. It is essential to make this distinction, because management and prognosis of these conditions are entirely different. A detailed history and, in some cases, special diagnostic methods can help make the diagnosis. When evaluating patients with anginalike chest pain and normal coronary arteries, physicians need to consider this group of diseases and tailor workup and diagnosis on an individual basis.

Changing characteristics of patients with vasospastic angina in the era of new calcium channel blockers.

In the 1980s, clinical characteristics and long-term prognosis of patients with vasospastic angina (VSA) were investigated; however, they remain to be updated after the introduction of new calcium channel blockers, benidipine and amlodipine, in 1990s. Our patient cohort registered 726 patients with VSA from January 1980 to December 2002. Before and after 1990, 138 and 527 patients were respectively entered in this study with a follow-up rate of 92%. Most of the patients were treated with calcium channel blockers, while benidipine and amlodipine were used in 28% and 21% of them only after 1990. Survival without cardiovascular events (96% versus 96%) at 5 years remained good before and after 1990. The presence of significant coronary stenosis had a negative prognostic impact both before and after 1990, whereas after 1990, diabetes mellitus, smoking, and a history of myocardial infarction became more influential. Among the calcium channel blockers, benidipine showed a better prognosis. These results suggest that in the era of new calcium channel blockers, the prognosis of patients with VSA remains good with more prognostic impact of diabetes mellitus, smoking, and a history of myocardial infarction and that benidipine might have some better prognostic effects.

[Prinzmetal's variant angina with transient complete atrio-ventricular block--case report]. / Napadowy blok calkowity z poronnymi zespolami MAS w przebiegu dlawicy naczynioskurczowej.

A case of 44-year-old women with episodes of chest pain with ST-T segment elevation and paroxysmal atrioventricular complete block with syncopal episodes is presented. Coronary angiography did not reveal atheromatous lesions. A patient was treated with nitrates and calcium channel blockers. However syncopal episodes with A-V block reoccurred. A single-chamber (ventricular demand) pacemaker was implanted. A six month follow-up was uneventful.

Menstrual cyclic variation of myocardial ischemia in premenopausal women with variant angina.

BACKGROUND: An abundance of ovarian hormones is assumed to be a major contributor to the low incidence of ischemic heart disease in premenopausal women. However, the effects of ovarian hormones remain undetermined. OBJECTIVE: To examine whether the variation in ovarian hormone levels throughout a menstrual cycle affects myocardial ischemia in women with variant angina. DESIGN: Prospective, observational study. SETTING: University medical center in Japan. PARTICIPANTS: 10 premenopausal women with variant angina. MEASUREMENTS: Frequency of spontaneous ischemic episodes, flow-mediated dilation of brachial artery, and serum levels of estradiol and progesterone. RESULTS: Frequency of ischemic episodes was highest from the end of the luteal phase to the beginning of the menstrual phase and was lowest in the follicular phase. Flow-mediated vasodilation and estradiol levels were lowest from the end of the luteal phase to the beginning of the menstrual phase and were highest in the follicular phase. CONCLUSIONS: In premenopausal women with variant angina, we documented a cyclic variation in endothelial function and the frequency of myocardial ischemia that was associated with the variation in estrogen levels.