MRI analysis of simple and aneurysmal bone cysts in the proximal humerus: what actually matters in clinical routine.

OBJECTIVE: To evaluate magnetic resonance imaging (MRI) characteristics of simple and aneurysmal bone cysts (SBC/ABC) of the proximal humerus and the intermittent difficulty in the imaging differentiation between the two in daily clinical routine. MATERIALS AND METHODS: MR images of 26 patients with suspected SBC/ABC in the proximal humerus were retrospectively assessed by two independent radiologists blinded to the final histological result. Based on a standard MRI protocol, different morphologic features and signal intensities of the lesion on non-enhanced and enhanced sequences were documented. The radiological diagnosis was correlated with histology. RESULTS: Eighteen patients had the image-based diagnosis of an SBC, yet the histology confirmed only 12, the residual 6 were identified as an ABC, despite the imaging criteria corresponding unambiguously to the former. One of the main reasons was the unicameral morphology of lesions, found in 9/14 (64.3%) cases of all ABCs, i.e., in 19/26 cases in total. Therefore, the sensitivity of the radiological diagnosis was moderate (57.14%), yet specificity very high (100%). In total, 69.2% (18/26) presented with a pathological fracture at admission, which correlated strongly with both circumferential (MCC = 0.65, p = 0.01) and septal (MCC = 0.42, p = 0.06) enhancement patterns. Circumferential enhancement was also found to correlate strongly with the histological diagnosis, being recognized in all cases of ABC (MCC = 0.44, p = 0.06). CONCLUSION: MRI characteristics of ABCs/SBCs in the proximal humerus are indifferent and ABCs may morphologically present as SBCs. Radiologists should be aware of the different, often confusing presentation of both entities in daily clinical routine.

Clinical applicability of coronary atherosclerotic lesion characterization.

Native coronary atherosclerosis (CAS) is a diffuse and progressive disease process that is occasionally associated with either clinical atherothrombosis and/or major adverse cardiac events (MACE) including: ST elevation myocardial infarction (STEMI), acute coronary syndromes without ST elevation (ACSWSTE), heart failure, cardiac arrest and sudden cardiac death. Both, the timing and coronary site responsible for the MACE are currently unpredictable. Cardiovascular investigators have engaged in the task of characterizing CAS lesions in order to enhance our knowledge of CAS pathophysiology. It was expected that the knowledge acquired will allow scientists and clinicians to develop effective strategies to detect and treat "vulnerable plaque" (VP) prior to the evolution of MACE. This review discusses the emerging data regarding the pathology and natural history of the VP and vulnerable patient and the progress made in characterizing atherosclerotic plaque instability and vulnerability. Future directions in the field of plaque characterization and their potential clinical and research applications are discussed.

Routine stress testing after percutaneous coronary interventions.

Percutaneous coronary intervention (PCI) is the most frequently performed cardiovascular procedure. Many physicians caring for post-PCI patients have routinely subjected patients to periodic stress testing. In the recent years, due to widespread use of drug eluting stents the combined rates of major adverse cardiac events (MACE) and in-stent restenosis (ISR) dropped <10% in the initial 12 months post-PCI, with only half of these patients bearing symptoms. This has translated into reduced pre-test probability of post-PCI ischemia. Consequently, the beneficial effect of this practice came into question. Moreover, in addition to its financial implications, routine post-PCI stress testing may carry potential harm: medication or exercise induced arrhythmia, infarction and/or death, patient irradiation exposure, false-positive tests resulting in excessive invasive testing or interventions, and the illusion of "wellness" in the face of a somewhat unpredictable disease. This review addresses the role stress testing post-PCI: it is concluded that routine stress testing in clinically stable asymptomatic post-PCI patients should be discouraged. Selective utilization of stress testing in patients with exceptionally high risk of ISR or MACE can be utilized to answer important clinical questions or guide and refine clinical care.

Aspirin for the prevention of cardiovascular morbidity.

Aspirin (ASA) use for secondary prevention in patients with cardiovascular (CV) disease is well established through its beneficial effects on the reduction of myocardial infarction, ischemic stroke and CV mortality. This beneficial effect of ASA seems to consistently outweigh the risk in most patient subsets. Current guidelines endorse ASA for primary prevention of CV events in adults who are at moderate-high risk of CV morbidity. Recent emerging data on the efficacy and safety of ASA conflicts with former randomized clinical trials and raises concerns regarding the validity of these recommendations. The following manuscript describes the data emerging from contemporary trials regarding the efficacy and safety of ASA in various patient subsets. The authors propose certain strategies to enhance safety and efficacy in order to augment the beneficial effects of ASA along with other modalities of primary prevention for suitable candidates. When contemplating ASA prescription for primary prevention of CV events, physicians should carefully weigh the potential benefits of risk reduction versus likelihood of harm, mostly related to bleeding complications.

Prescribing of psychotropic medication to the intellectually disabled by community paediatricians - a survey.

BACKGROUND: Children with intellectual disability are often managed by community paediatricians and have a high prevalence of mental disorder. We do not know whether community paediatricians feel adequately trained to treat this group although we know that paediatricians contribute significantly to psychotropic prescribing for children. METHODS: Psychotropic medication prescribing by community paediatricians to the intellectually disabled in the north-west and northern regions, community paediatricians' perceived training needs in this area and the availability of specialized psychiatric services were surveyed. Postal questionnaires were sent to all members of the British Association of Community Child Health in the north and north western regions (n= 155), between summer 2004 and autumn 2005. RESULTS: A total of 70.1% (n= 110) of questionnaires were returned of which 66 were completed. The most common reason for non-completion was that the respondent did not look after the intellectually disabled. A total of 54.5% of respondents did not have access to specialist psychiatry services for children and adolescents with an intellectual disability. Community paediatricians were most likely to prescribe for sleep disorders and attention deficit hyperactivity disorder (ADHD). There was a significant relationship between perceived adequacy of training and paediatrics prescribing for ADHD, but there was no such relationship for sleep disorders. The vast majority of community paediatricians did not feel adequately trained to prescribe for challenging behaviour or depression, although a small minority did prescribe. CONCLUSIONS: Community paediatricians play a substantial role in prescribing psychotropic medications for this group. A substantial minority of community paediatricians do not feel that they have enough training to prescribe for ADHD and sleep disorders, and perceived competency is more likely to inform prescribing for ADHD than for sleep disorders. This may have implications for training. Although these children pose complex difficulties, access to specialist mental health services for children and adolescents with intellectual disability remains patchy, especially in the north-west, and further development of these services is needed.

Arrhythmia susceptibility and myocardial composition in diabetes. Influence of physical conditioning.

Abnormal myocardial composition in diabetes mellitus has been described, but the effects on ventricular vulnerability have not been defined. We have assessed the susceptibility to arrhythmias in a canine model after 1 yr of mild diabetes induced by alloxan. Since physical conditioning can affect metabolic abnormalities in diabetes, this intervention has also been evaluated. Group 1 served as controls and groups 3 and 4 were diabetic. Animals in the latter group as well as nondiabetic controls of group 2 were exercised on a treadmill for the last 8 mo of the experiment. After 1 yr, anesthesia was induced with chloralose for vulnerability studies. The ventricular fibrillation threshold of 24.4 +/- 1.9 mA in group 3 was significantly less than in normals (45.1 +/- 2.2). Spontaneous arrhythmias were also more prevalent in diabetics during acute ischemia (group 3-A). Increased ventricular vulnerability after epinephrine infusion was present in the sedentary diabetes despite normal ventricular function responsiveness. In a superfused preparation of myocardium, resting membrane potential and action potential amplitude were normal in diabetics, and beta-adrenergic stimulation shortened repolarization more than in controls. Myocardial collagen concentrations, which included an interfibrillar distribution on morphologic examination, were increased in group 3. In the trained diabetics of group 4 the basal vulnerability thresholds and responses to epinephrine were normal. While myocardial collagen levels were normal, cholesterol and triglyceride increments persisted. Thus, in mild experimental diabetes, enhanced susceptibility to arrhythmias exists; this susceptibility may be based on a combination of nonhomogenous collagen accumulation affecting local conduction and increased electrophysiologic sensitivity to catecholamines.

In vivo myocardial cell pH in the dog. Response to ischemia and infusion of alkali.

Myocardial cell pH has been measured with 5,5-dimethyl-2,4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular, and water indicators were made into the anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady-state distribution of DMO between cells and plasma was calculated from the indicator mean transit times, and the plasma pH. Myocardial cell pH was determined from the distribution value and plasma pH. Normal myocardial cell pH averaged 6.94. Changes in myocardial cell pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a coronary artery balloon resulted in progressive decreases in cellular pH to average values of 6.83 within the initial 15 min and to 6.59 within the interval between 20 and 70 min. Infusions of Na2CO3 tended to diminish intracellular acidosis although these infusions had little effect on the difference in pH between the myocardial cell and extracellular fluid.

Myocardial function and lipid metabolism in the chronic alcoholic animal.

In view of the variables that obscure the pathogenesis of cardiomyopathy, a study was undertaken in mongrel dogs fed ethanol as 36% of calories for up to 22 mo. Both the experimental and control groups maintained body weight, hematocrit, plasma vitamin, and protein levels. Left ventricular function was evaluated in the intact anesthetized dog using indicator dilution for end-diastolic and stroke volume determinations. During increased afterload with angiotensin, the ethanol group exhibited a larger rise of end-diastolic pressure (P<0.01), whereas end-diastolic and stroke volume responses were significantly less than in controls. Preload increments with saline elicited a significantly higher end-diastolic pressure rise in the ethanol group (P<0.01). No hypertrophy, inflammation, or fibrosis was present and it was postulated that the enhanced diastolic stiffness was related to accumulation of Alcian Blue-positive material in the ventricular interstitium. To evaluate myocardial lipid metabolism, [1-(14)C]oleic acid was infused systemically. Plasma specific activity and myocardial lipid uptake were similar in both groups. There was a significantly increased incorporation of label into triglyceride, associated with a reduced (14)CO(2) production, considered the basis for a twofold increment of triglyceride content. In addition, diminished incorporation of [(14)C]oleic acid into phospholipid was observed accompanied by morphologic abnormalities of cardiac cell membranes. Potassium loss and sodium gain, like the lipid alteration, was more prominent in the subendocardium. Thus, chronic ethanol ingestion in this animal model is associated with abnormalities of ventricular function without evident malnutrition, analogous to the preclinical malfunction described in the human alcoholic.

Evidence for cardiomyopathy in familial diabetes mellitus.

Recent epidemiologic studies have suggested that cardiac disease in common in diabetics and may often have a noncoronary basis. To examine the status of the left ventricle, 17 adult-onset diabetics of familial type without hypertension or obesity underwent hemodynamic study and were compared to 9 controls of similar age. Of the 17, 12 subjects had no significant occlusive lesions by coronary angiography. From this group eight without heart failure had a modest, but significant, elevation of left ventricular end-diastolic pressure. End-diastolic and stroke volumes were reduced, but ejection fraction and mean rate of fiber shortening were within normal limits. The left ventricular end-diastolic pressure/volume ratio was significantly higher than controls. Afterload increments effected a significant increase of filling pressure compared to normals without a stroke volume response, consistent with a preclinical cardiomyopathy. Four patients with prior heart failure had similar but more extensive abnormalities. None had local dyskinesia by angiography, and lactate production was not observed during pacing-induced tachycardia. Left ventricular biopsy in two patients without ventricular decompensation showed interstitial collagen deposition with relatively normal muscle cells. These findings suggest a myopathic process without ischemia. Postmortem studies were performed in 11 uncomplicated diabetics. Nine were without significant obstructive disease of the proximal coronary arteries, and the majority succumbed with cardiac failure. On left ventricular sections, none had evident luminal narrowing of the intramural vessels. All nine exhibited periodic acid-Schiff-positive material in the interstitium. Collagen accumulation was present in perivascular loci, between myofibers, or as replacement fibrosis. Multiple samples of left ventricle and septum revealed enhanced triglyceride and cholesterol concentrations, as compared to controls. Thus, a diffuse extravascular abnormality may be a basis for cardiomyopathic features in diabetes.

Impact of symptomatic skeletal events on health-care resource utilization and quality of life among patients with castration-resistant prostate cancer and bone metastases.

BACKGROUND: Data regarding the impact of symptomatic skeletal events (SSEs) on health economics and patient-reported outcomes in men with castration-resistant prostate cancer (CRPC) and bone metastases from a clinical setting are lacking. Hence, this study aimed to quantify the effects of SSEs on health-care resource utilization (HRU), health-related quality of life (HRQoL) and pain in men with CRPC metastasized to bone. METHODS: This cohort study included men with CRPC and bone metastasis treated at a tertiary center during December 1996-July 2015. SSEs, including pathological fracture, radiation to bone, spinal cord compression and bone surgery, as well as HRU were identified retrospectively through medical records and clinical database. A subset of surviving patients completed Functional Assessment of Cancer Therapy-Prostate (FACT-P) and Brief Pain Inventory-Short Form (BPI-SF) questionnaires. The incremental effect of SSEs on HRU was evaluated using multivariable generalized linear regression. Questionnaire scores were compared using effect sizes (ES); ES⩾0.33 indicated meaningful differences between SSE and non-SSE cohorts. Lower scores suggest lower HRQoL and pain. RESULTS: Of the 832 patients, 207 developed ⩾1 SSE (mean 1.5±0.8) during follow-up (median 2.1 years). Radiation to bone was the most common SSE (84.1%). SSE cohort had significantly higher emergency room (incidence rate ratio (IRR)=1.48; P=0.006), outpatient (IRR=1.17; P=0.005) and inpatient (IRR=1.74; P<0.001) visits. Of the 107 eligible survey patients, 103 (96.3%) responded. SSE cohort had lower mean FACT-P functional well-being (17.5 vs 19.8; P=0.158; ES=0.36), higher mean pain severity (2.5 vs 1.6; P=0.048; ES=0.47) and worst pain scores (3.6 vs 2.3; P=0.033; ES=0.50) compared with the non-SSE cohort, indicating meaningful differences between cohorts. CONCLUSIONS: This study demonstrated high economic and HRQoL burden of SSEs. The findings underscore the need for better supportive and disease-modifying treatments for these patients.

Multiple-micronutrient supplementation for women during pregnancy.

BACKGROUND: Multiple-micronutrient deficiencies often coexist in low- to middle-income countries. They are exacerbated in pregnancy due to the increased demands, leading to potentially adverse effects on the mother. Substantive evidence regarding the effectiveness of multiple-micronutrient supplements (MMS) during pregnancy is not available. OBJECTIVES: To evaluate the benefits to mother and infant of multiple-micronutrient supplements in pregnancy and assess the risk of excess supplementation and potential adverse interactions between micronutrients. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (30 December 2005). SELECTION CRITERIA: All prospective randomised controlled trials evaluating micronutrient supplementation during pregnancy and its effects on the pregnancy outcome. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed trial quality and extracted the data. MAIN RESULTS: Nine trials (15,378 women) are included. When compared with supplementation of two or less micronutrients or no supplementation or a placebo, multiple-micronutrient supplementation resulted in a statistically significant decrease in the number of low birthweight babies (relative risk (RR) 0.83; 95% confidence interval (CI) 0.76 to 0.91), small-for-gestational-age babies (RR 0.92; 95% CI 0.86 to 0.99) and in maternal anaemia (RR 0.61; CI 0.52 to 0.71). However, these differences lost statistical significance when multiple-micronutrient supplementation was compared with iron folic acid supplementation alone. No statistically significant differences were shown for the outcomes of preterm births and perinatal mortality in any of the comparisons. A number of prespecified clinically important outcomes could not be assessed due to insufficient or non-available data from the included trials. These include placental abruption, congenital anomalies including neural tube defects, premature rupture of membranes, pre-eclampsia, miscarriage, maternal mortality, neurodevelopmental delay, very preterm births, cost of supplementation, side-effects of supplements, maternal wellbeing or satisfaction and nutritional status of children. AUTHORS' CONCLUSIONS: The evidence provided in this review is insufficient to suggest replacement of iron and folate supplementation with a multiple-micronutrient supplement. A reduction in the number of low birthweight and small-for-gestational-age babies and maternal anaemia has been found with a multiple-micronutrient supplement against supplementation with two or less micronutrients or none or a placebo, but analyses revealed no added benefit of multiple-micronutrient supplements compared with iron folic acid supplementation. These results are limited by the small number of studies available. There is also insufficient evidence to identify adverse effects and to say that excess multiple-micronutrient supplementation during pregnancy is harmful to the mother or the fetus. Further research is needed to find out the beneficial maternal or fetal effects and to assess the risk of excess supplementation and potential adverse interactions between the micronutrients.

Atosiban and nifedipine in acute tocolysis: a comparative study.

OBJECTIVE: The objective was to compare the effectiveness, efficacy, and safety of atosiban and nifedipine in preventing or delaying premature labor. DESIGN: An interventional, randomized, controlled trial of 63 women experiencing preterm labor varying from 24 to 35 completed weeks of gestation. The women were randomized to receive either atosiban intravenously (group I, n=31), or nifedipine orally (group II, n=32). RESULTS: There were no significant differences in effectiveness and efficacy of tocolysis between the two groups. Women with a history of preterm labor responded significantly better to atosiban than those with no such history. Those at 28 weeks or less responded significantly better to nifedipine, while those at more than 28 weeks' gestation showed an equal response in the two groups. Nifedipine achieved uterine quiescence in a significantly shorter time than atosiban. The maternal side effects were higher with nifedipine. Neonatal complications were comparable in both groups. CONCLUSIONS: Both drugs are equally effective and efficacious in acute tocolysis. Subgrouping of patients according to gestational age and history of preterm labor may be applied in selecting the line of treatment. The maternal side effects were higher with nifedipine.

Relation of platelets to catecholamine induced myocardial injury.

To test the thesis that myocardial injury, induced by catecholamines, is ischaemic in origin due to platelet accumulation in the coronary microvasculature, sustained left intracoronary and systemic infusion of catecholamines in toxic dosage was given to dogs previously infused with autologous 51Cr-labelled platelets. Subsequent determination of tissue radioactivity and electrolytes, as well as electronmicrography, indicated that the induced myocardial injury was not related to microvascular occlusion by platelets.

Cell sodium and the induction of myocardial injury after adrenaline.

Accumulation of calcium in cardiac cells during catecholamine induced injury is considered a major pathogenetic factor but its mechanism has not been defined. During initiation of injury in an intact canine model, cell sodium was enhanced fourfold in myocardium after a local infusion of epinephrine via the left anterior descending coronary artery for a 60 min period. Tissue calcium was enhanced and a major role for the Na-Ca carrier system is suggested. Regional myocardial function, blood flow and electrocardiogram responses to toxic levels of the catecholamine have been contrasted with ischaemic injury.

Ischemic heart failure: sustained inotropic response to small doses of I-epinephrine without toxicity.

As a prelude to a study of severe ischemic heart failure, the therapeutic response of the ischemic ventricle to epinephrine and acetylstrophanthidin in nontoxic doses was determined in 24 intact anesthetized dogs undergoing a first episode of acute regional ischemia. A thrombotic obstruction was produced in the left ventricular dysfunction. The elevation of end-diastolic pressure and reduced stroke volume in control dogs were not significantly altered by administration of strophanthidin. Epinephrine (0.05 mug/kg per min) elicited a significant reduction in end-diastolic pressure and increase in stroke volume. The latter was not attended by an increased incidence of ventricular fibrillation, whereas fibrillation occurred in half of the group given strophantihidin. Thus, the catecholamine was selected to study pump failure. Severe ischemic heart failure was assessed in two groups with scar from previous infarction for up to 4 hours. By 60 minutes of ischemia the increase in end-diastolic pressure and volume and decrease in stroke volume and ejection fraction were comparable in both groups. Thereafter, alternate animals received small doses of epinephrine (0.05 to 0.15 mug/kg per min) with graded increments at 60 minute intervals to counter tachyphylaxis and findings were compared with those in control dogs. Over the subsequent 3 hours, there was progressive deterioration of left anterior descending coronary artery, affecting ventricular function in the untreated group with an increase in end-diastolic pressure from 10 plus or minus 1 to 33 plus or minus 2.4 mm Hg. End-diastolic volume increased by 63 percent; stroke volume and ejection fraction decreased by 48 and 66 percent, respectively. The infusion of epinephrine was attended by a significantly lower end-diastolic pressure of 20 plus or minus 2.5 mm Hg, whereas end-diastolic volume, stroke volume and ejection fraction were restored to control levels after 4 hours of ischemia. Mortality in the untreated group was 62 percent by 4 hours; all seven animals in the treated group survived.

Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition.

Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.

Intra-aortic balloon counterpulsation in an experimental model of myocardial infarction.

The efficacy of intra-aortic balloon counterpulsation for heart failure during acute myocardial infarction has been controversial, and early intervention has been suggested as crucial. We have examined this type of therapy in the intact anesthetized dog during complete occlusion of the proximal left anterior descending coronary artery with a balloon-tipped catheter. Group 1 (n = 8) represented untreated animals undergoing four hours of ischemia. Group 2 (n = 7) consisted of animals undergoing counterpulsation with an intra-aortic balloon after 15 minutes of ischemia. Initially, stroke volume and the mean rate of left ventricular fiber shortening were similarly diminished in both groups, while filling pressure rose proportionately. After four hours, the mean rate of fiber shortening, stroke volume, and left ventricular filling pressure rose to a greater extent in untreated compared to treated animals (p less than 0.01). The degree of swelling in ischemic tissue and the number of sites with ST-segment elevation and their sums were comparable in the two groups. Thus, intra-aortic counterpulsation applied early in the course of ischemia can improve global left ventricular dysfunction without affecting the extent of myocardial injury.

Dietary vitamin B12 deficiency in an adolescent white boy.

Dietary deficiency of cobalamin resulting in tissue deficiency in white individuals is unusual. However, several patients with dietary deficiency who were neither vegan nor Hindu have been described. This report describes the case of a 14 year old boy who was a white non-Hindu with a very low intake of cobalamin, which was not apparent until a detailed dietary assessment was performed. The patient responded rapidly to a combination of oral and parenteral B12. This case illustrates the fact that severe dietary vitamin B12 deficiency can occur in non-Hindu white individuals. Inadequate dietary content of B12 may not be apparent until a detailed dietary assessment is performed. This patient is likely to have had subclinical vitamin B12 deficiency for several years. Increased vitamin B12 requirements associated with the adolescent growth spurt may have provoked overt tissue deficiency.

Efficacy and safety of combinations of nitrendipine, atenolol, and hydrochlorothiazide in black hypertensive patients.

Twenty-four black hypertensive patients were studied in a randomized, double-blind trial of combinations of nitrendipine, atenolol, and hydrochlorothiazide. After six weeks, blood pressure was normalized in all three treatment groups, i.e. diastolic blood pressure less than 95 mmHg and a decline in diastolic blood pressure of at least 5 mmHg from baseline. The drug combinations containing hydrochlorothiazide were associated with higher incidence of metabolic abnormalities, especially hypokalaemia and hyperuricaemia.

Myocardial infarction postpartum in patients taking bromocriptine for the prevention of breast engorgement.

Three cases of myocardial infarction (MI) in women taking bromocriptine for milk suppression are presented. The incidents occurred in 1993 and 1994, the last only two weeks before the withdrawal of the drug from the American market as a drug suitable for ablactation. In one patient, the MI presented on the 12 day postpartum and was accompanied by signs and symptoms reminiscent to ergotism. Another mother suffered MI, accompanied by hypertension, six days after a vaginal delivery complicated by postpartum haemorrhage. The third patient began to take bromocriptine more than 2 weeks postpartum and died suddenly 24 days after her childbirth. To the knowledge of the authors, these are the 12th to 14th literary reports describing an apparent association between the use of bromocriptine for ablactation and the occurrence of MI in the puerperium.