Acute myocardial infarction and coronary vasospasm associated with the ingestion of cayenne pepper pills in a 25-year-old male

Capsaicin, one of the major active components of cayenne pepper pills, is an over-the-counter substance with sympathomimetic activity used commonly by young individuals for weight loss. Here we report the case of a previously healthy young male who developed severe chest pain after using cayenne pepper pills for slimming and sustained an extensive inferior myocardial infarction. Electrocardiography combined with a bedside transthoracic echocardiogram confirmed the diagnosis of acute myocardial infarction. The patient denied using illicit substances, and he had no risk factors for coronary artery disease. His medication history revealed that he had recently started taking cayenne pepper pills for slimming. A subsequent coronary angiogram revealed patent coronary arteries, suggesting that the mechanism was vasospasm. We postulate that the patient developed acute coronary vasospasm and a myocardial infarction in the presence of this known sympathomimetic agent. This case highlights the potential danger of capsaicin, even when used by otherwise healthy individuals

Clinical and histologic studies of a Qatari family with myofibrillar myopathy

The current Study reports the first family with confirmed rnyofibrillar myopathy (MFM) in the Middle East and the third family worldwide. This Study highlights the importance of considering MFM in Young patients presenting with idiopathic cardiomyopathy, arrhythmia or atrioventricular block in the Gulf states. This is the first report that presented 2 different types of cardiomyopathy and 2 different indications of permanent pacemaker placement in the same Generation of a family with MFM. This report studies a Qatari family consisting of one brother and 3 sisters. The brother had restrictive cardiomyopathy at the age of 16 years. One sister underwent heart transplantation for severe hypertrophic cardiomyopathy at the age of 15 years, the other sister had permanent pacemaker for complete heart block at the age of 21 years. This report is focused mainly on the clinical presentation and investigations carried out for the brother including echocardiogram, cardiac catheterization, cardiac and skeletal muscle biopsy, and electromyography and electrophysiology studies. The Study findings Support the diagnosis of MFM

Mechanisms of coronary artery spasm

The term coronary artery spasm (CAS) refers to a sudden, intense vasoconstriction of an epicardial coronary artery that causes vessel occlusion or near occlusion. Although CAS may be involved in other coronary syndromes, it represents the usual cause of variant angina. The variant form of angina was first described in 1959 by Prinzmetal et al,1 who used this term to indicate that angina attacks, unlike the most common form of effort angina, occurred at rest and were associated with ST-segment elevation, rather than ST-segment depression, on the ECG (Figure 1). Because myocardial ischemia occurred in the absence of any change in myocardial oxygen demand, the authors hypothesized that it was caused by an increased tonus of vessels at the level of coronary stenoses.1 Some years later, in fact, coronary angiography, performed during spontaneous angina attacks, demonstrated that CAS is the usual cause of variant angina.2 4 Coronary angiography also showed that CAS could occur at the site of a stenosis (either minor or severe) or in angiographically normal coronary arteries,5 usually at a localized segment of an epicardial artery (focal spasm) (Figure 2).6 However, sometimes CAS involves 2 or more segments of the same (multifocal spasm) or of different (multivessel spasm) epicardial coronary arteries, or may also involve diffusely one or multiple coronary branches.7 Careful assessment of clinical history and 24- to 72-hour ambulatory ECG monitoring are usually sufficient to achieve the diagnosis of variant angina, whereas the use of provocative tests of CAS (eg, intravenous ergonovine, intracoronary ergonovine, or acetylcholine administration) is required in about 10% of patients.7 Transmural myocardial ischemia caused by occlusive CAS can be complicated by malignant ventricular arrhythmias,8,9 which can result in sudden death, or, if prolonged, by acute myocardial infarction.10 Accordingly, a prompt diagnosis would be essential to prevent these serious complications, even though calcium antagonists are very effective in preventing CAS.11,12 However, the diagnosis of variant angina is often overlooked for several months after its manifestation.7 Sixty years after the first description of variant angina, the causes and the mechanisms of CAS are still poorly defined. The research in this field has indeed been refrained by several factors, including the low incidence of the disease and the considerable efficacy of nonspecific vasodilator therapy.12 However, in 10% to 20% of patients, CAS is refractory to standard treatment, or high doses of calcium antagonists are needed to effectively prevent its recurrence. Thus, elucidating the mechanisms responsible for CAS could make treatment of difficult or refractory cases easier.13 In this article, we review the state of knowledge regarding the etiopathogenesis of CAS in patients with the clinical syndrome of Prinzmetal variant angina

The effect of high plasma levels of angiotensin-converting enzyme (ACE) and plasminogen activator inhibitor (PAI-1) on the reperfusion after thrombolytic therapy in patients presented with acute myocardial infarction

The resistance to thrombolytic agents and delays in reperfusion occur in more than 30% after acute myocardial infarction. This may play an important role in the unsuccessful recanalization after thrombolytic therapy. The aim of this study is to assess the clinical and biochemical markers of reperfusion after different types of thrombolytic therapy and to find out the relationship between PAI-1 and ACE serum levels and the short-term outcome. Pretreatment ACE and PAI-1 plasma levels of 184 patients with acute myocardial infarction, treated with thrombolytic therapy were determined. Failure of thrombolysis was considered when reperfusion was delayed as assessed by noninvasive reperfusion criteria, reinfarction, and impaired left ventricular function. High plasma level of ACE (> 50 U/L), PAI-1 (> 43 ng/ml) and both was found in 57, 108 and 32 patients respectively. Subjects with high ACE plasma levels were characterized by impaired LV systolic function (79.0% vs. 75.0%), new Q-wave (88.4% vs. 74.2%), less reperfusion arrhythmia (19.3% vs. 22.8%) and prolonged hospitalization (70% vs. 66%) but no statistical significance was observed. High enzymes levels of PAI-1 were observed with higher incidence of anterior myocardial infarction (50.0% vs. 41.0%), lesser ST segment resolution (65.6% vs. 58.8%), reinfarction (6.3% vs. 5.9%), and impaired LV systolic function (90.6% vs. 76.0%), and prolonged hospitalization (70.4% vs. 63.4). There was a statistically significant difference between thrombolytic agents in the presence of high ACE regarding hospital overstay (p = 0.02). While the presence of high PAI-1 was significantly affect the degree of ST-segment resolution (p = 0.03)

Epidemiology of idiopathic cardiomyopathy in Qatar during 1996-2003

Objectives: To report the rates of cardiomyopathies in the population below 50 years of age in Qatar. Subjects and Methods: We conducted a retrospective review of clinical data on patients with cardiomyopathy who were hospitalized in Hamad General Hospital, Doha. Data were collected from medical records during the 1996 2002 period and prospectively from the patients who were hospitalized during the year 2003. All cardiomyopathy patients below 50 years of age who were citizens or permanent residents in Qatar were included in this study. Results: During the study period, a total of 132 cases were recorded with idiopathic cardiomyopathies. Among these, 67.4% were males and 32.6% females; Qatari 31.8%, non-Qatari 68.2%. The consanguinity rate was high among Qatari patients. In the first 7-year study period, 1996 - 2002, the incidence rate of all types of cardiomyopathies was 2.5/100,000 population per year (95% CI: 1.4 - 3.5). It increased to 5.2/100,000 population during the year 2003 (95% CI: 3.6 - 6.7). Dilated cardiomyopathy was most prevalent (75.8%) in all age groups, and the incidence increased remarkably with age. Lower prevalence of hypertrophic cardiomyopathy (13.6%) and left ventricle noncompaction cardiomyopathy (6.1%) was found. In children below 15 years of age, the incidence rate for all types of cardiomyopathies was 2.7/100,000 population. The overall mortality rate was 5.3%. Conclusion: Most cases of cardiomyopathy were identified at an early age: below 15 years and above 35 years of age. Introducing preventive and early diagnosis programs may have an impact on reducing the mortality and morbidity from idiopathic cardiomyopathy. Copyright (C) 2006 S. Karger AG, Basel