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Patient: Male, 51Final Diagnosis: ST-segment elevation myocardial infarction with acute stent thrombosisSymptoms: Chest pain • hiccupsMedication: —Clinical Procedure: —Specialty: CardiologyObjective:Unusual clinical courseBackground:Acute coronary syndrome (ACS) can present with atypical chest pain or symptoms not attributed to heart disease, such as indigestion. Hiccups, a benign and self-limited condition, can become persistent or intractable with overlooked underlying etiology. There are various causes of protracted hiccups, including metabolic abnormalities, psychogenic disorders, malignancy, central nervous system pathology, medications, pulmonary disorders, or gastrointestinal etiologies. It is rarely attributed to cardiac disease.Case Report:We report a case of intractable hiccups in a 51-year-old male with cocaine related myocardial infarction (MI) before and after stent placement. Coronary angiogram showed in-stent thrombosis of the initial intervention. Following thrombectomy, balloon angioplasty, and stent, the patient recovered well without additional episodes of hiccups. Although hiccups are not known to present with a predilection for a particular cause of myocardial ischemia, this case may additionally be explained by the sympathomimetic effects of cocaine, which lead to vasoconstriction of coronary arteries.Conclusions:Hiccups associated with cardiac enzyme elevation and EKG ST-segment elevation before and after percutaneous coronary intervention (PCI) maybe a manifestation of acute MI with or without stent. The fact that this patient was a cocaine user may have contributed to the unique presentation.

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A 40-year-old man with a medical history of hypertension was admitted for weight loss, generalised weakness, joint pains and mottling of fingertips. The initial laboratory data revealed microangiopathic haemolytic anaemia, thrombocytopenia and acute renal failure. Intravenous steroids were started for possible diagnosis of systemic lupus erythematosus based on admission assessment. Intravenous immunoglobulin and plasmapharesis were subsequently added to the treatment plan to cover thrombotic thrombocytopenic purpura while his autoimmune panel was pending. The echocardiogram study on day 2 revealed cardiac tamponade for which he underwent pericardiocentesis and right heart catheterisation. The atrial waveforms postpericardiocentesis demonstrated effusive-constrictive pericarditis. His clinical condition kept on deteriorating with reaccumulation of pericardial effusion and further complicated by hemoperitoneum and colonic obstruction. He had cardiorespiratory arrest on his fourth admission day and was not revived. Anti-Scl-70 antibody came back positive. Autopsy findings confirmed the presence of fibrinous pericarditis and hemoperitoneum.

Background: Risk of cardiovascular events is higher in patients with chronic kidney disease. The objective is to evaluate whether glomerular filtration rate (GFR) on admission is an independent predictor of short-term mortality in acute myocardial infarction (AMI), after adjusting with physiologic derangements in an acute setting. Methods: 220 consecutive patients with an admitting diagnosis of AMI were enrolled in a 1-year prospective observational study at a tertiary care teaching institute. Data were gathered for history, physical examination and laboratory findings. GFR was calculated based on the Modification of Diet in Renal Disease formula. Abnormal categories of physiological derangement indicators were weighted based on APACHE II guidelines. The endpoint was defined as in-hospital all-cause mortality. Results: There were 31 deaths (14.1%). The GFR (mean ± SD) in survivors as compared to deceased patients was 68.2 ± 33.8 and 41.7 ± 25.1 ml/min/1.73 m², respectively (p < 0.001). The mean age, white blood cell count, blood urea nitrogen, potassium and blood sugar were higher on admission in patients who died in hospital (p < 0.05), while the mean albumin, mean arterial pressure, pulse and respiratory rate were lower in this group compared to survivors (p < 0.05). After adjusting with other covariates, each 10 ml/min/1.73 m² decrease in GFR was associated with a 1.29 times increased risk of mortality (95% CI 1.08–1.53, p = 0.004). Conclusion: GFR on admission is an independent predictor of short-term mortality in a patient after AMI.

The case is reported of a yoga practitioner who, during an exacerbation of asthma, developed a substantial increase in serum muscle enzymes. This was related to his yoga breathing exercises, which he used to enhance the delivery of aerosolised bronchodilators. As his condition improved and the use of these yoga manoeuvres diminished, the muscle enzyme levels fell to normal.Mild to moderate increase in serum creatine kinase and other muscle enzyme activities have been reported with both acute and chronic asthma,'-3 and independently with the regular practice of yoga.45 Substantial increases in muscle enzymes have not been reported in either of these conditions alone or in combination. Case reportsA 63 year old yoga enthusiast with a two year history of asthma was admitted with shortness of breath and wheezing of one week's duration. His asthma had been well controlled with oral theophylline (300 mg thrice daily), salbutamol tablets (8 mg thrice daily), and a beclomethasone inhaler. He claimed that yoga breathing exercises usually alleviated mild attacks of wheezing. On this occasion, however, the exercises were not effective.Physical examination showed laboured breathing at 32 breaths a minute, a hyperresonant chest, and bilateral diffuse wheezing.The initial peak expiratory flow (PEF) was 450 1/min, whereas he knew his usual value to be 800 1/min. Arterial blood gas analysis when he was breathing 2 1/min of oxygen by nasal cannula showed a pH of 7 45, an arterial carbon dioxide tension of 4-4 kPa, and an arterial oxygen tension of 7-6 kPa. The chest radiograph was normal. An electrocardiogram showed sinus tachycardia and was unchanged from the previous one.Treatment for asthma was begun with an aminophylline infusion, methylprednisolone, nebulised orciprenaline, and oral salbutamol.On admission serum creatine kinase activity was 777 IU/1, lactic dehydrogenase 207 IU/1, aspartate aminotransferase 37 Address for correspondence: Dr Frank M Tamarin, Division of Pulmonary Diseases, New Rochelle Hospital, New Rochelle, New York, USA. Reprints will not be available. Accepted 23 March 1988 IU/1, and aldolase 49 U/I (normal < 8 U/1). Creatine kinase activity continued to rise and peaked on the second day with a value of 2273 IU/I (figure). Isoenzyme analysis showed the creatine kinase and lactic dehydrogenase to originate only from skeletal muscle. Tests for serum rheumatoid factor and antinuclear antibody gave negative results and the urine was free of myoglobin. Creatinine clearance was 99 ml/min. The results of thyroid function tests and the erythrocyte sedimentation rate were normal. The peak flow increased to 550 1/min by the fourth hospital day.The origin ofthe increased serum muscle enzyme activities was not clear in the absence of muscle pain, seizure activity, and trauma. When specifically questioned about vigorous physical activity the patient denied conventional exercise but demonstrated his yoga breathing manoeuvres, which consisted offorceful repetitive undulating movements, beginning in the legs...

Inappropriate elevations in plasma aldosterone levels have multiple actions that play an important role in the pathophysiology of hypertension and heart failure. Patients with hypertensive cardiovascular disease are at increased risk for coronary artery disease, myocardial infarction, congestive heart failure, and sudden cardiac death. Despite long-term treatment with an angiotensin converting enzyme inhibitor or an angiotensin II receptor blocker, aldosterone levels usually remain high in these patients. The effectiveness of low-dose spironolactone raises the possibility that a nonselective aldosterone antagonist can block the deleterious effects of aldosterone on the cardiovascular system. However, side effects limit the use of this drug in many patients. The advent of selective aldosterone antagonists, which have a lower affinity for androgen and progesterone receptors, should minimize these side effects, leading to better compliance.