[Apical ballooning syndrome, case series]. / Broddthensluheilkenni--sjúkratilfelli og yfirlit.

Apical ballooning syndrome is a cardiac syndrome typically characterized by transient focal dyskinesia or akinesia of the mid and apical regions of the left ventricle and hyperkinesia of the basal region. The symptoms and signs of the patient mimic myocardial infarction, with chest pain, electrocardiographic changes and elevation of cardiac enzymes but without significant coronary artery disease. The syndrome is frequently preceded by physical or emotional stress. We describe three cases of apical ballooning syndrome diagnosed during 10 days in December 2007 at Landspítali University Hospital Reykjavík.

Classic intermittent claudication is an uncommon manifestation of lower extremity peripheral arterial disease in hospitalized patients with coronary artery disease.

Synchronous peripheral arterial disease (PAD) and coronary artery disease (CAD) is common. Standardized questionnaires such as the Rose/WHO questionnaire and later the Edinburgh modification of this questionnaire were developed to screen for PAD. Little data are available on the sensitivity of these questionnaires in hospitalized patients with CAD. The aim of this study was to determine the accuracy of these questionnaires and the prevalence of classic intermittent claudication in hospitalized patients with CAD. Medically stable patients with CAD were invited to participate before hospital discharge. The patients answered both the Rose/WHO and Edinburgh modification claudication questionnaires and had an ankle-brachial index (ABI) measured. An ABI less than or equal to 0.9 was considered to be indicative of significant PAD. Patients who had undergone previous lower extremity revascularization for PAD and had a corrected ABI greater than 0.9 were excluded. Ninety-five patients (66 men) were recruited. By measuring the ABI, 35 patients (25 men) were found to have significant PAD. An additional 3 patients who had an ABI corrected by lower extremity revascularization were excluded from the analysis. The Rose/WHO questionnaire had a sensitivity, specificity, and overall accuracy (95% CI) of 14.3% (2.7-25.9%), 96.7% (92.1-100%), and 66.3% (56.8-75.8%), respectively. The Edinburgh modification of the Rose/WHO questionnaire had a sensitivity, specificity, and overall accuracy (95% CI) of 28.6% (13.6-43.5%), 90.0% (82.4-97.6%), 67.4% (57.9-76.8%), respectively. Despite the high incidence of synchronous PAD in hospitalized patients with CAD, traditional claudication questionnaires are insensitive to PAD detection. Classic claudication is an uncommon manifestation of PAD in hospitalized patients with CAD.

Use of a percutaneous vascular suture device for closure of an inadvertent subclavian artery puncture.

A well-known complication of central venous catheterization is inadvertent arterial sheath placement. Sheath removal from noncompressible arteries has the potential for severe complications. We report a case of inadvertent subclavian arterial sheath placement during an attempted internal jugular venous catheterization. This was successfully removed using a percutaneous vascular suture device.

Lower extremity peripheral arterial disease in hospitalized patients with coronary artery disease.

The prevalence of coronary artery disease (CAD) in patients with peripheral arterial disease (PAD) has been well defined. However, the prevalence of PAD in hospitalized patients with CAD has not been defined. The ankle-brachial index (ABI) is a useful non-invasive tool to screen for PAD. The aim of our study was to assess the prevalence of PAD in hospitalized patients with CAD by measuring the ABI. The study was conducted at the University of Wisconsin Hospital and Clinics inpatient Cardiovascular Medicine Service. Medically stable patients with CAD were invited to participate prior to hospital discharge. Data regarding cardiovascular risk factors, history of previous PAD, physical examination, and ABI were collected. An ABI less than or equal to 0.9 or a history of previous lower extremity vascular invention was considered to be indicative of significant PAD. A total of 100 patients (66 men and 34 women) were recruited. Forty patients were found to have PAD (mean ABI in non-revascularized patients with PAD = 0.67). By measuring the ABI, 37 (25 men) were positive for PAD and three had an ABI corrected with previous revascularization. Of these patients, 21 (52.5%) had previously documented PAD. Patients with PAD were older (p = 0.003), had a greater smoking history (p = 0.002), were more likely to have diabetes (p = 0.012), hypertension (p = 0.013) and a trend towards more dyslipidemia (p = 0.055). In conclusion, hospitalized patients with CAD are likely to have concomitant PAD. Risk factors for PAD in this patient population include advanced age, history of smoking, diabetes, hypertension, dyslipidemia and abnormal pulse examination. Identification of patients with PAD by measuring the ankle-brachial index is easily done.

Relation of "inotropic reserve" to functional capacity in heart failure secondary to ischemic or nonischemic cardiomyopathy.

Exercise capacity in patients with dilated cardiomyopathy, measured by peak oxygen consumption (VO(2)) during exercise, has virtually no relation to resting left ventricular (LV) function. We hypothesized that exercise-induced inotropic reserve may explain some of the variation between peak VO(2) and resting LV function. Treadmill stress echocardiography was performed simultaneously with peak VO(2) measurements in 35 patients with dilated cardiomyopathy. Resting and immediate postexercise echocardiographic images were scored for change in segmental contractility using the American Society of Echocardiography 16-segment system. Segment scores were summed and divided by 16 to determine the wall motion index. Right ventricular (RV) function was quantified on a 4-point scale. Patients had a mean age of 52 +/- 12 years (8 women) and a mean ejection fraction of 30 +/- 10 (25 nonischemic patients). Average peak VO(2) was 17.0 +/- 6 ml/kg/min. Patients were divided into 2 groups by peak VO(2): a high VO(2) group, >17 ml/kg/min (17 patients) and a low VO(2) group, < or =17 ml/kg/min (18 patients). LV ejection fraction was similar between the high and low VO(2) groups (31 +/- 9% vs 28 +/- 11%, p = NS) as were etiology of heart failure, medications used, and LV volume. In the high VO(2) group, wall motion index improved from 2.28 +/- 0.20 to 2.12 +/- 0.31 during exercise (p = 0.009). There was no improvement in the low VO(2) group. Resting RV function was significantly better in the high VO(2) group (1.4 +/- 0.8 vs 0.6 +/- 0.6 p = 0.004). Therefore, in patients with dilated cardiomyopathy and similar resting LV function, the presence of demonstrable LV inotropic reserve and preserved RV function partially account for variation in exercise performance.