A Case Report and Literature Review of Spontaneous Perforation of Pyometra.

BACKGROUND: Pyometra is defined as an accumulation of purulent material in the uterine cavity. Spontaneous perforation is a very rare complication of pyometra. The clinical findings of perforated pyometra are similar to perforation of the gastrointestinal tract and other causes of acute abdomen. CASE REPORT: We report a rare and difficult case of peritonitis in an elderly female that was caused by a spontaneous perforation of pyometra. A 90-year-old postmenopausal woman was referred to our hospital with complaints of vomiting, fever, and abdominal pain. Computed tomography revealed a large amount of ascites, cystic mass in the uterus, and intraperitoneal and intrauterine air. Transvaginal ultrasound demonstrated a thin area around the fundus. An emergency laparotomy was performed for the suspected gastrointestinal perforation or perforation of pyometra. At laparotomy, copious purulent fluid was present in the peritoneal cavity; however, no perforation of the gastrointestinal tract was observed. We identified a perforation site over the uterine fundus and purulent material exuding from the cavity. Subsequently, hysterectomy and bilateral salpingo-oophorectomy were performed. The patient was discharged on postoperative day 13 with no complications. Histopathologic studies revealed endometritis and myometritis with no evidence of malignancy. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: With diffuse peritonitis, ruptured pyometra should be considered, even in elderly female patients. This case illustrates the importance of clinical knowledge of acute gynecologic diseases. Here we also review the perforation of pyometra with no evidence of malignancy.

Impact of sirolimus-eluting stent fracture on 4-year clinical outcomes.

BACKGROUND: Although stent fracture (SF) after sirolimus-eluting stent (SES) implantation has been recognized as one of the predisposing factors of in-stent restenosis, it remains uncertain whether SF can increase the risk of major adverse cardiac events (MACE), especially beyond 1 year after SES implantation. The aim of this study was to assess the impact of SF relative to non-SF on 4-year clinical outcomes after treatment with SES of comparable unselected lesions. METHODS AND RESULTS: A total of 874 lesions in 793 patients undergoing SES implantation and subsequent angiography 6 to 9 months after index procedure were analyzed. At 6- to 9-month angiographic follow-up, SF was identified in 70 of 874 lesions (8.0%). In-stent late loss was significantly higher in SF lesions versus non-SF lesions (0.42±0.59 mm versus 0.13±0.49 mm, P<0.001), resulting in a significantly higher in-stent restenosis rate (21.4% versus 4.1%, P<0.001). At 4 years, SF versus non-SF was associated with a significantly higher MACE rate (23.2% versus 12.6%, P=0.014), mainly driven by significantly higher target-lesion revascularization (18.8% versus 10.2%, P=0.029) rate. Adverse effects of SF on clinical outcomes occurred mostly within the first year (17.4% versus 6.6%, P=0.001), with similar MACE rate between 1 and 4 years (5.8% versus 5.9%, P=0.611). No significant differences between SF versus non-SF patients were observed in the cumulative frequency of very late stent thrombosis (2.9% versus 1.4%, P=0.281), death (0% versus 2.1%, P=0.252), or myocardial infarction (5.8% versus 2.9%, P=0.165). CONCLUSIONS: SF of SES was associated with higher MACE rate up to 1 year, mainly driven by higher target-lesion revascularization, whereas no significant association was evident between years 1 and 4.

Subtle myocardial damage associated with diagnostic coronary angiography alone.

AIMS: To evaluate the frequency, predictors and prognostic significance of elevation in cardiac troponin I (cTnI) after coronary angiography (CAG). METHODS AND RESULTS: A series of 296 consecutive patients with normal pre-procedural cTnI levels and undergoing elective CAG at our centre were prospectively analysed. Positive cTnI elevation was defined as >0.06 ng/ml. Positive cTnI elevation was observed in 44 patients (14.8%), but CK-MB was elevated in only four patients (1.3%) after the procedure. The risk of cTnI elevation was independently associated with left ventricular hypertrophy (odds ratio [OR] 5.52; 95% confidence interval [CI], 2.54 to 12.02; P<0.001), inexperienced operator (OR 10.83; 95% CI, 2.47 to 47.43; P=0.002) and the amount of contrast agent (OR 1.12; 95% CI, 1.03 to 1.23; P=0.009 for each 10 ml increase), whereas it was not associated with the severity of coronary artery disease. At one year, however, postprocedural elevation of cTnI was not associated with an increased risk of death (2.3% vs. 0.8%, P=0.384) or myocardial infarction (2.3% vs. 2.0%, P=0.623). CONCLUSIONS: A minor elevation of cTnI is observed commonly after CAG, which might be associated with left ventricular hypertrophy, operator's experience and the amount of contrast used; however, it does not influence 1-year events rates.

Relationship between severity of renal impairment and 2-year outcomes after sirolimus-eluting stent implantation.

BACKGROUND: The presence of chronic kidney disease (CKD) is associated with an increased risk of restenosis and major adverse cardiac events (MACEs) after coronary interventions, especially in patients on hemodialysis (HD). The aim of this study was to assess the impact of varying degrees of renal impairment on angiographic and 2-year clinical outcomes after treatment with sirolimus-eluting stents (SESs). METHODS: A total of 675 lesions of 593 patients treated with SES were analyzed. Patients were classified into 3 groups: 34 patients on HD; 337 patients with estimated glomerular filtration rate > or =60 mL min(-1) 1.73 m(-2) (non-CKD group); and 222 patients who had lower estimated glomerular filtration rate <60 mL min(-1) 1.73 m(-2) without HD dependency (CKD group). RESULTS: At angiographic follow-up (201 +/- 73 days), in-segment late loss was markedly higher in the HD group versus the non-CKD and CKD groups (0.68 +/- 1.06 vs 0.11 +/- 0.45 and 0.15 +/- 0.50 mm, respectively, P < .001), resulting in a significantly higher in-segment restenosis rate (40.0% vs 10.4% and 11.5%, respectively, P < .001). At 2 years, HD vs non-CKD and CKD was associated with a significantly higher MACE rate (35.3% vs 10.4% and 12.6%, respectively, P < .001), mainly driven by significantly higher mortality (11.8% vs 0.6% and 2.3%, respectively, P < .001) and target-lesion revascularization (23.5% vs 9.2% and 8.1%, respectively, P = .016) rates. Multivariable analysis revealed that HD was the independent predictor of 2-year MACE (hazard ratio 4.70, 95% CI 2.40-9.20, P < .001). CONCLUSIONS: Although angiographic and clinical outcomes after SES implantation were similarly favorable in non-HD-dependent CKD patients, regardless of renal function, in patients with end-stage CKD requiring HD, frequencies of restenosis and 2-year MACE were markedly higher than in non-HD-dependent patients.

Diversity of the elevation of serum cardiac troponin I levels in patients during their first visit to the emergency room.

BACKGROUND: Although measurement of serum creatine kinase levels, as well as myoglobin levels, has been used for screening patients with acute coronary syndrome (ACS), the specificity of both is low. Measurement of cardiac troponin levels is now extensively used for the diagnosis of ACS because of their superior cardiac specificity. However, troponin levels are reportedly elevated not only in patients with ACS but also in those with other diseases. METHODS AND RESULTS: The clinical characteristics of 1,023 patients (mean age: 63.5+/-16.3 years; males: 665, females: 358) whose serum cardiac troponin I (cTnI) levels had been measured at the initial visit to the emergency room of Toyota Memorial Hospital between April 2004 and March 2005 were retrospectively analyzed. A positive elevation of cTnI was defined as cTnI > or =0.03 ng/ml. There were 432 patients (42.2%) with positive cTnI levels. The cTnI levels (8.48+/-2.64 ng/ml) in patients with acute myocardial infarction (AMI) were greater than those (0.25+/-0.07 ng/ml) in patients with unstable angina pectoris (AP), as well as those (0.04+/-0.01 ng/ml) in patients with stable AP. In terms of the diagnosis of AMI, the sensitivity was high enough (94.6%), but its specificity was relatively low (61.9%). Furthermore, the differentiation between AMI and unstable AP by the cTnI value alone was impossible. The cTnI levels were elevated in patients with a variety of diseases other than ACS, including heart failure, cardiomyopathies, myocarditis, renal failure, tachyarrhythmias, and pulmonary embolism. CONCLUSIONS: Elevation of the cTnI level is frequently observed in patients in the emergency room with common diseases other than ACS.

Relationship between exercise-induced myocardial ischemia and reduced left ventricular distensibility in patients with nonobstructive hypertrophic cardiomyopathy.

UNLABELLED: Many studies have demonstrated that reduced left ventricular (LV) diastolic distensibility plays a key role in the pathophysiology of hypertrophic cardiomyopathy (HCM). However, the relationship between myocardial ischemia and reduced LV distensibility in HCM remains unclear. We aimed to clarify the relationship between exercise-induced ischemia and reduced LV distensibility in patients with HCM. METHODS: Twenty patients with HCM and 5 age-matched control subjects underwent stress-redistribution (201)Tl myocardial scintigraphy and biventricular cardiac catheterization and echocardiography at rest and during exercise. Scintigraphic defect analysis was interpreted using Berman's 20-segment model. The summed stress score (SSS) was calculated as the sum of scores of the 20 LV segments and the summed difference score (SDS) was calculated as the sum of differences between each of the 20 LV segments on stress and rest images. RESULTS: Patients were divided into 2 groups according to the (201)Tl defect as follows: 9 patients with an SSS on (201)Tl of >or=10 and an SDS on (201)Tl of >or=5 (ischemic group) and 11 patients with an SSS of <10 or an SDS of <5 (nonischemic group). The absolute increases from rest to peak exercise in LV end-diastolic pressure (LVEDP) and pulmonary artery wedge pressure were significantly greater (15.5 +/- 5.2 vs. 7.6 +/- 5.5 mm Hg and 17.3 +/- 5.0 vs. 8.9 +/- 5.0 mm Hg, P < 0.01, respectively), and the percentage changes from rest to peak exercise in the maximum first derivative of LV pressure and LV pressure half-time were significantly smaller in the ischemic HCM group compared with the nonischemic HCM group (70% +/- 24% vs. 123% +/- 43% and -32% +/- 6.4% vs. -44% +/- 9.4%, P < 0.01, respectively). However, the end-diastolic dimensions did not differ between the 2 HCM groups. One of the 9 patients in the ischemic group, as revealed by fill-in on (201)Tl scintigraphy, showed increased (18)F-FDG uptake in the anteroseptal wall. CONCLUSION: Some HCM patients show a significant increase in LVEDP without chamber dilatation, indicating reduced LV diastolic distensibility. Myocardial ischemia may at least in part contribute to this condition.

Effect of nicorandil on left ventricular end-diastolic pressure during exercise in patients with hypertrophic cardiomyopathy.

AIMS: Impaired coronary microcirculation is thought to contribute to myocardial ischaemia, causing an abnormal increase in left ventricular end-diastolic pressure during exercise in individuals with hypertrophic cardiomyopathy. The effects of nicorandil on left ventricular end-diastolic pressure during exercise were examined in patients with this condition. METHODS AND RESULTS: Left ventricular pressures and dimensions were measured simultaneously during supine bicycle exercise in 23 patients with nonobstructive hypertrophic cardiomyopathy, before and after intravenous injection of either nicorandil (0.1 mg/kg) or propranolol (0.15 mg/kg). Exercise thallium-201 scintigraphy was also performed. Patients were grouped according to the changes in left ventricular end-diastolic pressure during exercise before treatment. Group I comprised 13 patients in whom left ventricular end-diastolic pressure increased progressively to abnormal values during exercise; group II comprised 10 patients in whom left ventricular end-diastolic pressure changed biphasically. The extents of both left ventricular hypertrophy and ischemic burden during exercise were greater in group I than in group II. Of the eight group I patients who received nicorandil, four individuals exhibited biphasic changes in left ventricular end-diastolic pressure during exercise after its administration whereas four subjects showed no such effect of the drug. Left ventricular end-diastolic pressure increased progressively during exercise after propranolol treatment in all 6 group II patients given this drug. CONCLUSION: Nicorandil has a salutary effect on the changes in left ventricular end-diastolic pressure during exercise in patients with hypertrophic cardiomyopathy.