Variant angina induced by carbon monoxide poisoning: A CARE compliant case report.

RATIONALE: Carbon monoxide (CO) poisoning can cause severe damage to the nervous system, and can also cause serious damage to organs, such as the heart, kidneys, and lungs. CO damage to myocardial cells has been previously reported. This can lead to serious complications, such as myocardial infarction. PATIENT CONCERNS: A 47-year-old female patient complained of sudden chest pain for 30 minutes. Before admission, the patient had non-radiating burning chest pain after inhalation of soot. DIAGNOSIS: An electrocardiogram showed that myocardial ischemia was progressively aggravated, manifested by progressive ST-segment elevation, and accompanied by T wave inversion and other changes. No obvious coronary stenosis was observed in a coronary angiographic examination. Therefore, the patient was considered to have developed variant angina resulting from CO poisoning-induced coronary artery spasm. INTERVENTIONS: The patient was treated with drugs for improving blood circulation and preventing thrombosis, and underwent hyperbaric oxygen therapy. OUTCOMES: Clinical symptoms relieved after the treatment. LESSONS: Findings from this case suggest that CO can cause coronary artery spasm and it is one of the predisposing factors of variant angina. For these patients, hyperbaric oxygen therapy can improve blood circulation and prevent formation of thrombus and encephalopathy.

Pharmacotherapy of Vasospastic Angina.

Vasospastic angina is a diagnosis of exclusion that manifests with signs and symptoms, which overlap with obstructive coronary artery disease, most often ST-segment elevation myocardial infarction. The pharmacotherapy that is available to treat vasospastic angina can help ameliorate angina symptoms. However, the etiology of vasospastic angina is ill-defined, making targeted pharmacotherapy difficult. Most patients receive pharmacotherapy that includes calcium channel blockers and/or long-acting nitrates. This article reviews the efficacy and safety of the pharmacotherapy used to treat vasospastic angina. High-dose calcium channel blockers possess the most evidence, with respect to decreasing angina incidence, frequency, and duration. However, not all patients respond to calcium channel blockers. Nitrates and/or alpha1-adrenergic receptor antagonists can be used in patients who respond poorly to calcium channel blockers. Albeit, evidence for use of nitrates and alpha1-adrenergic receptor antagonists in vasospastic angina is not as robust as calcium channel blockers and can exacerbate adverse effects when added to calcium channel blocker therapy. Despite having a clear benefit in patients with obstructive coronary artery disease, the benefit of beta-adrenergic receptor antagonists, statins, and aspirin remains unclear. More data are needed to elucidate whether or not these agents are beneficial or harmful to patients being treated for vasospastic angina. Overall, the use of pharmacotherapy for the treatment of vasospastic angina should be guided by patient-specific factors, such as tolerability, adverse effects, drug-drug, and drug-disease interactions.

A case of variant angina in a patient under chronic treatment with sorafenib.

BACKGROUND: A 63-year-old man with an unresectable multifocal hepatocellular carcinoma (HCC) presented with upper abdominal discomfort, nausea and vomiting. We report a case of variant angina in a patient affected by unresectable HCC under chronic treatment with sorafenib. Spontaneous spasm occurred during cardiac catheterization and was revealed during coronary angiogram with the unusual feature of a retrograde transient filling of a contralateral branch. INVESTIGATIONS: Electrocardiogram, cardiac catheterization, chest X-ray, emergency ECG. DIAGNOSIS: Variant angina induced by sorafenib treatment mimicking infero-posterior ST-elevation myocardial infarction (STEMI). MANAGEMENT: High-dose calcium-antagonists and nitrates were initially given intravenously and then orally. Sorafenib therapy was then resumed without further symptoms. Restaging of the cancer revealed unexpected local recurrence and the patient died 1 month after receiving palliative care. We contend that the effects of sorafenib treatment were primarily responsible for the major cardiovascular event observed in this case, and it is important for clinicians to be aware of this possible severe complication of sorafenib therapy.

[Extraction, combination and distribution regularity of syndrome elements in patients with variant angina pectoris].

OBJECTIVE: To explore the pathogenesis characteristics of variant angina pectoris (VAP) by extracting its syndrome elements and analyzing the combination and distribution regularity of the syndrome elements. METHODS: One hundred and seventy-five case files of VAP patients were collected. The extraction of syndrome elements and symptom contribution to syndrome was completed by the partition method of complex system based on entropy theory. Diagnostic threshold was established by receiver operator characteristic curve. According to the results diagnosed by diagnostic criteria for syndrome element with quantitation, the combination and distribution regularity of the syndrome elements in patients with VAP was analyzed. RESULTS: The basic syndrome elements in the patients with VAP were qi deficiency, qi stagnation, blood stasis, phlegm turbidity, phlegm-heat, stagnation-heat, yin deficiency and yang deficiency syndromes. It showed that the combination types of syndrome elements could be made up of one syndrome, two, three, four or more than four syndromes. Qi deficiency, yin deficiency, qi stagnation, blood stasis and phlegm turbidity syndromes had the higher frequency than other syndrome elements in the patients with VAP. CONCLUSION: The partition method of complex system based on entropy theory can be used in extracting the syndrome elements of the patients with VAP. It is found that VAP has complicated pathogenesis according to the combination and distribution regularity of syndrome elements. Qi deficiency, qi stagnation, blood stasis, phlegm turbidity and yin deficiency syndromes are the main syndrome elements.

Variant angina associated with bitter orange in a dietary supplement.

The Food and Drug Administration has banned the sale of ephedrine-based weight-loss products because of their association with many cardiovascular adverse effects. Bitter orange is now being used as a stimulant in "ephedra-free" weight-loss supplements but was recently implicated in adverse cardiovascular sequelae. To our knowledge, this report describes the first case of variant angina associated with bitter orange in a dietary supplement.

Multivessel variant angina unresponsive to urapidil.

We present a case of variant angina complicated by recurrent sudden cardiac death. During coronary angiography a diffuse 3-vessel vasoconstriction was observed progressing to a more severe vasoconstriction in the mid LAD. Intracoronary administration of urapidil did not reverse the vasoconstriction of the LAD; instead an occlusive vasospasm occurred accompanied by marked ischaemia.

Prinzmetal's angina.

Prinzmetal's angina, often referred to as "variant" angina, is a temporary increase in coronary vascular tone (vasospasm) causing a marked, but transient reduction in luminal diameter. This coronary vasospastic state is usually focal at a single site and can occur in either a normal or diseased vessel. Patients are predominantly younger women who may not have the classical cardiovascular risk factors (except for cigarette use). PVA has been associated with vasospastic disorders such as Raynaud's phenomenon and migraine headaches. Arrhythmias are common and may be life threatening especially when the effects of vasospasm are seen in those ECG leads that reflect the potential variations of the epicardial surface of the left ventricle. Endothelial dysfunction has been considered as primarily responsible for PVA. The diagnosis is made by observing transient ST-segment elevation during the attack of angina. Since PVA is not a "demand"- induced symptom, but rather a supply (vasospastic) abnormality, exercise treadmill stress testing is of no value in the diagnosis of PVA. The most sensitive and specific test for PVA is the administration of ergonovine intravenously. Fifty micrograms at 5-minute intervals is given until a positive result or a maximum dose of 400 microg has been administered. When positive, the symptoms and associated ST-segment elevation should be present. Nitroglycerin rapidly reverses the effects of ergonovine if refractory spasm occurs. Medical therapy classically employs vasodilator drugs, which include nitrates and calcium channel blockers. The prognosis is good when there is no significant coronary artery stenosis. Treatment of associated coronary atherosclerosis in elderly patients with PVA is advised. When PVA is associated with coronary atherosclerosis, the prognosis is determined by the severity of the underlying disease. beta-Blockers and large doses of aspirin are contraindicated in PVA.

[The placement of a Wiktor stent for the treatment of vasospastic angina: a case report]. / Colocación de stent de Wiktor para el tratamiento de angina vasoespástica: presentación de un caso.

A 46-year-old male with a fixed stenosis in the mid-segment of the left anterior descending artery underwent balloon angioplasty. The procedure included the placement of two Wiktor stents because of severe dissection. Five months later he complained of Prinzmetal angina with ST elevation in the anterior wall. A metilergobasine test during the coronary arteriogram showed a discrete, severe spasm on the proximal segment of the left anterior descending artery. Because of a lack of symptomatic improvement with high-dose nitrates and calcium blockers, a Wiktor coronary stent was successfully implanted in the proximal left anterior descending artery, resulting in complete relief of the angina.

Normas de diagnóstico clínico de gabinete y tratamiento del infarto agudo de miocardio y sus variantes

Se enfatiza en la importancia del cuadro clínico exámenes de laboratorio y de gabinete en el diagnóstico de la Cardiopatía Isqúémica: Angina de pecho estable y/o inestable, Infarto Agudo del Miocardio clásico y/o silente, el Síndrome Intermedio y la variante del Prinzmetal. Se analiza el cuadro clínico, la exploraciónfísica, el electrocardiograma, las isoenzimas cardiacas, la valoración por radioisótopos, la radiología, el ecocardiograma modo M, modo B, el Doppler pulsado, el cateterismo cardiaco y la angiografía. Se toma en cuenta en la conducta terapéutica, las medidas generales: analgesia y sedación, la oxigenoterapia, anticoagulacíon, la profilaxis antifibrilatoria ventricular, el manejo de la Insuficiencia Cardiaca (clasificación clínica de Killip y hemodinámica de Forrester). En Angina Inestable su concepto, etiología, diagnóstico, examen físico, ECG, Rx, ergometría, cuantificación de músculo isquémico por ecocardiografía (prueba de dipiridamol-Talio), la valoración hemodinámica por cateterismo cardíaco, el diagnóstico diferencial, y el tratamiento farmacológico y/o quirúrgico. Finalmente se analiza la Cariopatía Isquémica Crónico igualmente con sus parámetros clínicos, exploracíon física, ECG, de reposo y ejercicio, perfusión miocárdica con Talio 201, función ventricular con Tecnecio 99, el ecocardiograma, el monitoreoholter, y el tratamiento a base de nitratos, bloqueadores beta adrenérgicos, calcioantagonistas, y antiagregantes plaquetarios, enfatizando la importancia del intervencionismo radiológico: angioplastia transluminal coronaria, y/o la cirugía de revascularización miocárdica por fuentes venosas.

[Characteristics of traditional Chinese medicine syndromes in both spontaneous and variant angina. An analysis of 21 cases].

An analysis of TCM syndromes is reported in 21 cases with both spontaneous and variant angina as compared with 147 cases with effort angina. The results showed that 3 characteristic features were present, which were as follows: the Biao-Shi syndrome of cold condensation was more than that of the control group in ratio of 42.86% to 3.40%; the Ben-Xu syndrome of Yang deficiency was more and that of Qi deficiency less than those in the control group, and they were in ratio of 33.33% to 6.12% and 33.33% to 72.11% respectively. An absolute reduction of blood supply resulted from coronary spontaneous spasm in both spontaneous and variant angina causes severe chest pain during attacks as a cold condensation type. Hyperfunction of parasympathetic nerves often occurring in coronary heart disease with Yang deficiency is liable to vasoconstriction of the large coronary arteries leading to episodes of both spontaneous and variant angina. The presence of less Qi deficiency type may be related to the less impairment of cardiac function resulted from the short course in these cases and only relatively mild state of an illness, even no marked lesion in coronary arteries in a part of patients with both spontaneous and variant angina. No significant difference in TCM syndromes occurred between spontaneous and variant angina. Both Yang and Yin deficiency, as the Ben-Xu syndromes, were more present in angina of cold condensation type.(ABSTRACT TRUNCATED AT 250 WORDS)

Spontaneous remission of variant angina documented by Holter monitoring and ergonovine testing in patients treated with calcium antagonists.

Twenty-four patients with Prinzmetal's variant angina showing a favorable initial response to calcium antagonist treatment were studied to assess the evolution of the disease and the frequency and time course of spontaneous remission. At 3, 6 and 12 months from the acute phase, patients underwent in-hospital control studies, with 48-hour Holter monitoring and ergonovine testing carried out during treatment and after its interruption. During calcium antagonist therapy complete protection from spontaneous attacks was documented in 22 of 24 patients at 3 months, in 19 of 21 at 6 months and in all 21 at 12 months; ergonovine test results were negative in 16 of 23 patients at 3 months, in 16 of 20 at 6 months and in all 20 studied at 12 months. After stopping treatment spontaneous attacks did not reappear in 7 of 24 patients (29%), 14 of 21 (66%) and 16 of 21 (76%) at 3, 6 and 12 months respectively, while the ergonovine test response remained negative in 6 of 21 (28%), 7 of 18 (39%) and 13 of 20 (65%) of the patients controlled at 3, 6 and 12 months. Thus, complete remission of angina documented by both Holter recording and ergonovine testing occurred in 5 of 24 patients (21%) at 3 months, in 7 of 21 (33%) at 6 months and in 12 of 21 (57%) at 12 months. Patients with remission of angina had a shorter duration of symptoms and more often showed normal or not critically diseased coronary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasospastic angina: control of disease activity and efficacy of drug treatment using the prolonged hyperventilation test.

Sixteen consecutive patients with vasospastic angina underwent a control provocation test in the coronary care unit or the cardiac catheterization laboratory in order to evaluate the disease activity and the efficacy of long-term calcium antagonist treatment. In patients without angina at rest, the prolonged hyperventilation test was negative in 10/10 patients on calcium antagonist treatment (group A + B) and in 4/5 patients without medication (group C). The test was positive in 1/1 patient with angina at rest without medication (group D). However, the test provoked vasospastic angina in 1/5 patients who were asymptomatic without medication. In both the latter patients the prolonged hyperventilation test became negative after the restart of calcium antagonist treatment. During a mean follow-up period of 18 months (range 16-19) after the control hyperventilation test, no relapse of angina at rest, arrhythmias, syncopes, deaths or myocardial infarctions were registered. Thus, a negative test is compatible with low disease activity and/or efficacy of calcium antagonist treatment. Further, the test may reveal a subclinical tendency to coronary artery spasm.

[Comparative study of the effectiveness of korinfar, izoptin and obzidan in patients with variant stenocardia combined with effort stenocardia]. / Sravnitel'noe izuchenie éffektivnosti korinfara, izoptina i obzidana u bol'nykh s variantnoi stenokardiei, sochetaiushcheisia so stenokardiei napriazheniia.

Twelve patients with variant angina combined with angina of effort were examined. Repeated exercise tests prior to the administration of antianginal drugs revealed the spontaneous variability of the patients' tolerance to the exercise and of the pulse-pressure index at the exercise peak which may serve as an indirect sign of the angiospastic factor involvement in clinical manifestations of angina of effort. The treatment of such patients with corinfar and isoptin was associated with the elimination and significant reduction of spontaneous attacks of angina attended by a considerable increase in the exercise tolerance and in the pulse-pressure index at the exercise peak. The treatment with obsidan in these cases was less effective: the incidence of spontaneous anginal attacks changed insignificantly, the tolerance to exercise increased with the reduction of the maximum value of the pulse-pressure index.

Ergonovine provocation to assess efficacy of long-term therapy with calcium antagonists in Prinzmetal's variant angina.

In the patient with Prinzmetal's variant angina, the response to therapy with calcium antagonists may be assessed symptomatically, electrocardiographically (that is, by ambulatory electrocardiographic monitoring), or by response to ergonovine provocation. Although some studies have suggested a good relation between anginal frequency and ergonovine responsiveness in these patients, none has compared ambulatory electrocardiographic activity with the results of ergonovine provocation during the long-term administration of calcium antagonists. Therefore, the present study was performed to compare ergonovine responsiveness with both clinical and ambulatory electrocardiographic activity in patients with Prinzmetal's variant angina during long-term therapy with placebo, verapamil, and nifedipine. Accordingly, 27 patients with variant angina (19 men and 8 women, mean age 52 years) received placebo and verapamil for 2 months each, after which 23 of the 27 also received nifedipine for 2 months. All patients kept a diary of chest pains, and all had weekly 24-hour 2-channel ambulatory electrocardiographic (Holter) monitoring, from which episodes of transient S-T segment deviation were quantitated. During the final week of therapy with each agent, ergonovine was administered, beginning at 0.025 mg and incrementally increasing to 0.20 mg. It was discontinued when the patient had chest pain with S-T segment elevation greater than or equal to 0.1 mV or received a total dose of 0.50 mg. Of the 74 tests, 59 were negative; 6 of the negative tests occurred during a treatment period in which the patient had greater than 10 chest pains/week and greater than 25 episodes of S-T segment deviation/week. Of the 15 positive tests, 8 became positive during administration of less than 0.20 mg ergonovine; 5 of the positive tests occurred during a treatment period in which the patient had no chest pain or S-T segment deviation. Thus, in patients with variant angina, disease activity cannot be monitored reliably by ergonovine provocation because some patients have negative ergonovine tests at a time of marked clinical and electrocardiographic activity, whereas others have positive tests at a time of little (or no) disease activity.

Verapamil therapy for Prinzmetal's variant angina: comparison with placebo and nifedipine.

This study was performed (1) to assess the efficacy and safety of verapamil in patients with variant angina, and (2) to compare verapamil and nifedipine in patients with this clinical syndrome. In 27 patients, placebo and verapamil were administered in a long-term randomized, and double-blind study of 9 months' duration. In comparison to placebo, verapamil reduced the frequency of angina, nitroglycerin usage, transient episodes of electrocardiographic S-T segment deviation (as assessed by 2-channel Holter monitoring), and hospitalizations required for clinical instability. Subsequently, 23 patients were treated with nifedipine in a nonblind fashion for 2 months, and this agent exerted a beneficial effect similar to that of verapamil. Finally, gated equilibrium blood pool scintigraphy, performed in 10 patients at rest and during exercise during treatment with placebo, verapamil, and nifedipine, demonstrated that neither calcium antagonist caused a deterioration of left ventricular performance. Thus, (1) long-term oral verapamil and nifedipine are each superior to placebo and are of similar efficacy in patients with variant angina, and (2) neither agent adversely influences left ventricular performance in patients with relatively normal left ventricular function.

The hyperventilation test as a method for developing successful therapy in Prinzmetal's angina.

In 10 cases of Prinzmetal's angina in which episodes of myocardial ischemia were easily and reproducibly induced by hyperventilation, this test was performed 111 times, 41 times under control conditions and 70 times during treatment with one or more of the following drugs: phentolamine, isosorbide dinitrate, propranolol, verapamil, nifedipine and amiodarone. Seventeen of 18 negative tests performed under the influence of a long-acting drug coincided with total remission of the patient's anginal episodes when this drug was administered on a short- or long-term basis. No patient died or sustained infarction during a follow-up period of 10.9 months. A negative test was thus a good indication that the clinical response to the corresponding drug would be favorable. The electrocardiographic changes and chest pain provoked by hyperventilation occurred not when alkalosis was greatest (hydrogen ion [pH] change from 7.42 to 7.58, p less than 0.001), but when pH was approaching normal or control values. The onset of electrocardiographic changes occurred an average of 175 seconds after the end of hyperventilation and, in two cases, the time lag was as much as 480 and 705 seconds, respectively. This raises several questions regarding the true mechanism triggering coronary spasm under such conditions. The hyperventilation test appears to be a useful and safe procedure for selecting the best possible drug for long-term treatment of Prinzmetal's angina as well as for comparing the relative efficacy of different drugs.