Acute myocarditis secondary to Campylobacter jejuni enteritis: A case report.

Acute myocarditis is a rare complication of Campylobacter jejuni enteritis. Herein, we report the case of a 20-year-old man who presented with chest pain that developed three days after the onset of enteritis. Electrocardiogram, echocardiogram, and cardiac enzyme levels suggested myocarditis. Cardiac magnetic resonance imaging revealed a late gadolinium enhancement in the inferior wall. Degeneration and necrosis of myocardial cells and lymphocyte-dominant inflammatory cell infiltration were found in the tissue obtained by endomyocardial biopsy. Acute myocarditis associated with C. jejuni enteritis was confirmed by these findings and C. jejuni detected in the stool culture. The symptoms of enteritis and myocarditis remitted 10 days after the onset. The left ventricular ejection fraction was improved from 40 % to 57 %.In previous cases, endomyocardial biopsy has not been performed because of mild myocarditis. The lack of pathological reports makes the mechanism of myocarditis associated with C. jejuni enteritis unknown. We report a case of myocarditis associated with C. jejuni enteritis, which was diagnosed using cardiac magnetic resonance imaging and endomyocardial biopsy. Learning objective: Acute myocarditis is a rare but important complication of Campylobacter jejuni enteritis. Cardiac magnetic resonance imaging is useful for diagnosis. Most cases of myocarditis associated with C. jejuni enteritis were mild and remitted without specific treatment. In the present case, endomyocardial biopsy was performed and CD4-positive lymphocytes were predominantly detected in the myocardial tissue.

Right ventricular mural infective endocarditis after traumatic tricuspid valve regurgitation in a 40-year-old man: A case report.

As the clinical manifestations of traumatic tricuspid valve regurgitation vary according to the extent of tricuspid valve injury, this condition can often go unnoticed and be incidentally discovered. Here, we report the case of a 40-year-old man with patent foramen ovale, in which severe tricuspid regurgitation due to tricuspid valve prolapse was incidentally discovered following blunt chest trauma. Further examination revealed that the prolapse had also caused active right ventricular mural infective endocarditis. The patient had no relevant past medical history of chronic debilitating disease or immunosuppression. After evaluation by the cardiology team, emergent surgical tricuspid valvular repair was successfully performed. Learning objective: Tricuspid valve prolapses resulting from chest trauma may occasionally lead to severe tricuspid regurgitation. Furthermore, this may cause active right ventricular infective endocarditis. In the present case, Staphylococcus aureus was detected in blood cultures, which is usually rapidly progressive and often leads to devastating consequences. Early surgical approach should be considered in cases of infection in the left atrium via patent foramen ovale.

Balloon angioplasty for uncontrollable hypertension caused by coral reef aorta: A case report.

Coral reef aorta is a stenosis of the aorta due to severe calcification. We report the case of a 74-year-old woman with coral reef aorta whose hemodynamics were physiologically similar to those found in patients with renovascular hypertension. The patient had resistant hypertension, refractory edema, and renal dysfunction. Bilateral renal artery stenosis and infrarenal aortic stenosis were suspected after a Doppler ultrasound examination. Evaluation by intravascular ultrasound and pressure wire revealed that the high blood flow caused by infrarenal aortic stenosis derived from the high-flow velocity in a renal artery without stenosis. Angioplasty with balloon improved the stenosis, and the patient was relieved from a spiral of uncontrollable hypertension, edema, and renal dysfunction. This rare case was a patient with coral reef aorta who was diagnosed with uncontrollable hypertension and angioplasty was performed effectively and minimally invasively. .

Prediction of distal embolization during percutaneous coronary intervention for unstable plaques with grayscale and integrated backscatter intravascular ultrasound.

OBJECTIVES: We performed microscopic examination of the debris collected by a distal protection device and investigated the usefulness of grayscale and integrated backscatter intravascular ultrasound (IB-IVUS) for the prediction of distal embolization during percutaneous coronary intervention (PCI) in cases of unstable angina. BACKGROUND: The prediction of distal embolization during PCI has not been studied in depth because assessment of distal embolization is difficult. METHODS: We prospectively studied 39 consecutive patients with unstable angina who underwent PCI with a filter distal protection device. The preprocedural plaque volume at target lesions was measured with grayscale IVUS and plaque characteristics were assessed with IB-IVUS. We performed microscopic examination of the particles collected by the distal protection device. RESULTS: There was a significant correlation between the plaque volume and the number of the collected particles >100 µm in diameter (r = 0.48, P = 0.0034). Filter no-reflow (FNR) phenomenon was found in nine patients. The plaque volume was significantly greater (355 ± 133 mm(3) vs. 199 ± 90 mm(3) , P = 0.0004), and the lipid ratio was significantly higher (29.3 ± 4.3% vs. 26.1 ± 4.3 P = 0.045) in the FNR group compared with the non-FNR group. Multivariate logistic regression analysis showed that the plaque volume was an independent predictor of FNR phenomenon. CONCLUSIONS: Although tissue characterization of IB-IVUS may provide additional information for distal embolization, plaque volume is the only significant predictor of distal embolization during PCI.

Effect of embolic particles during coronary interventional procedures on regional wall motion in patients with stable angina pectoris.

Microembolization during percutaneous coronary intervention (PCI) causes minor myocardial injury, and a Doppler guidewire can detect embolic particles as high-intensity transient signals (HITS). The present study investigated the effect of microembolization during PCI on regional wall motion using a Doppler guidewire and myocardial strain analysis. We performed PCI to the left anterior descending coronary artery in 25 patients (18 men and 7 women, 68 ± 8 years old) with stable angina pectoris. Coronary flow spectrums were obtained with a Doppler guidewire to count the total number of HITS throughout the PCI procedures. On the days before and after PCI, we recorded echocardiography and measured the longitudinal peak systolic strain, peak strain rate, and early diastolic strain rate in the left anterior descending territory using a 2-dimensional speckle tracking method. PCI was successfully performed, and 10 ± 6 HITS (range 0 to 22, median 9) were recognized during PCI. The echocardiographic study showed no visible wall motion abnormalities in the left anterior descending territory either after or before PCI. In cases in which the total number of HITS was ≥10, the peak systolic strain, peak strain rate, and early diastolic strain rate worsened on the day after PCI compared with those on the day before PCI (p <0.01). The rates of change in peak systolic strain and early diastolic strain rate, defined as the ratios of those parameters after PCI to those before PCI, had modest to strong inverse correlations with the total number of HITS (R(2) = 0.35 and R(2) = 0.46, respectively). In conclusion, periprocedural microembolization during PCI reduces subclinical cardiac function in patients with stable angina pectoris.

Third in-stent restenosis in sirolimus eluting stents: predictors of the next restenosis.

OBJECTIVES: We evaluated the predictive factors for recurrent restenosis lesions treated on two previous occasions with sirolimus-eluting stents (SES). BACKGROUND: Angiography data related to recurrent SES restenosis have not been reported. METHODS: Binary restenosis was observed in 66 patients with 78 lesions from a total of 1,393 patients with 1,965 lesions who received follow-up angiography after SES implantation. We enrolled 55 patients with 67 lesions who underwent revascularization using another SES with a second follow-up coronary angiography. These restenotic lesions were divided into two groups based on the presence or absence of recurrent restenosis: no recurrent restenosis group (n = 56) and recurrent restenosis group (n = 11). The coronary angiography data during first and second SES implantation were compared between the groups. RESULTS: Minimal lumen diameter (MLD) was smaller before first and second percutaneous coronary interventions (PCI) with SES implantation in the recurrent restenotic group compared with no recurrent restenosis group (first PCI, 0.28 ± 0.19 mm vs. 0.54 ± 0.42 mm, P = 0.040; second PCI, 0.44 ± 0.36 mm vs. 0.69 ± 0.39 mm, P = 0.036, respectively). Acute stent recoil after second SES implantation was significantly greater in the recurrent restenosis group compared with no recurrent restenosis group (0.08 ± 0.17 mm vs. 0.20 ± 0.22 mm, P = 0.049, respectively). Multivariate analysis showed preprocedural MLD at first PCI and acute stent recoil at second PCI as independent predictors of recurrent restenosis. CONCLUSIONS: Preprocedural smaller MLD at first PCI and acute stent recoil at second PCI are predictors of recurrent restenosis treated on two previous occasions with SES.

Effect of elevated left ventricular diastolic filling pressure on the frequency of left atrial appendage thrombus in patients with nonvalvular atrial fibrillation.

We investigated the relation between left ventricular diastolic dysfunction and left atrial appendage (LAA) thrombus in patients with atrial fibrillation (AF). We performed transesophageal echocardiography to examine LAA thrombus or spontaneous echo contrast (SEC) and to measure LAA emptying flow velocity in consecutive 376 patients with AF. We estimated diastolic filling pressure as the ratio of early transmitral flow velocity (E) to mitral annular velocity (e') on transthoracic echocardiogram. E/e' ratio in 28 patients (7.4%) with LAA thrombi was higher than that in patients without thrombus (18.3 ± 9.3 vs 11.4 ± 5.9, p <0.0001). The fourth quartile of E/e' (>13.6) consisted of 19 patients with thrombi and had a higher prevalence of thrombi than the others (p <0.0001). Multivariate regression analysis selected E/e' ≥13 as an independent predictor of LAA thrombus with an odds ratio of 3.50 (1.22 to 10.61) in addition to LA dimension and ejection fraction. Increased quartile of E/e' was negatively associated with LAA flow velocity and positively with rate of SEC. In conclusion, increased diastolic filling pressure is associated with a higher rate of LAA thrombus in AF, partly through blood stasis or impaired LAA function.

Automated assessment of myocardial viability after acute myocardial infarction by global longitudinal peak strain on low-dose dobutamine stress echocardiography.

BACKGROUND: Low-dose dobutamine stress echocardiography (DSE) assesses myocardial viability at the early stage of acute myocardial infarction (AMI), but its assessment is subjective and variable. Automated function image (AFI) determines global longitudinal peak strain (GLPS) based on tissue tracking technique. The ability of GLPS obtained by AFI during dobutamine stress to assess myocardial viability after AMI was investigated. METHODS AND RESULTS: Low-dose DSE at day 3 in 23 consecutive patients with AMI was performed using Vivid 7 (GE Healthcare). Segmental longitudinal peak strain with AFI and obtained GLPS was analyzed. Wall motion score index (WMSI) by echocardiography 1 month later was determined. In 18 patients, left ventriculography was also performed at 3.2±1.5 months later to obtain left ventricular ejection fraction (LVEF) and regional wall motion (RWM, SD/chord). GLPS was improved during dobutamine infusion at 10 µg · kg(-1) · min(-1) (-12.9 ± 3.5% to -15.2 ± 3.6%, P=0.0004). GLPS during dobutamine stress showed good correlations with follow-up WMSI (R=0.47, P=0.02), with peak CK-MB (R = 0.52, P=0.01), with RWM (R = -0.48, P=0.04), and with LVEF (R = -0.54, P=0.02), whereas GLPS at baseline showed no correlations with them. Averaged segmental peak strain at baseline and during stress were correlated with follow-up WMSI (R = 0.50 and 0.43, respectively), but not with LVEF. CONCLUSIONS: GLPS during dobutamine stress determined by AFI is a promising, objective index to assess myocardial viability on the early stage of AMI.

Nicorandil treatment in patients with acute myocardial infarction: a meta-analysis.

BACKGROUND: It is controversial as to whether nicorandil would have cardioprotective effects in patients with acute myocardial infarction (AMI) who are undergoing reperfusion therapy. A meta-analysis was performed to study the impacts of nicorandil on functional outcomes after AMI. METHODS AND RESULTS: Randomized prospective cohort or retrospective cohort publications were identified up to October 2007 by means of a computer search of MEDLINE and Google Scholar databases. Two reviewers checked the quality of the studies and extracted data regarding patient and disease characteristics, study design, functional parameters such as Thrombolysis In Myocardial Infarction (TIMI) flow grade after reperfusion, left ventricular ejection fraction (LVEF) and left ventricular end-diastolic volume index (LVEDVI). Seventeen studies were included for the meta-analysis in this study. Nicorandil treatment reduced the incidence of TIMI flow grade < or =2 in 1,337 patients of 10 studies (risk ratio 0.63; 95% confidence interval (CI) 0.44 to 0.91). While no beneficial effect was observed on the peak creatine kinase value, nicorandil treatment was associated with greater LVEF (by 3.7%, 95%CI 1.8 to 5.7%), and lower LVEDVI (by 8.8 ml/kg, -14.4 to -3.3 ml/kg) in 905 patients of 11 studies. CONCLUSIONS: The meta-analysis demonstrated that nicorandil treatment adjunctive to reperfusion therapy has beneficial effects on microvascular function and on functional recovery after AMI.

Comparison of two- versus three-dimensional myocardial contrast echocardiography for assessing subendocardial perfusion abnormality after percutaneous coronary intervention in patients with acute myocardial infarction.

Myocardial contrast echocardiography (MCE) visualizes myocardial perfusion abnormalities after acute myocardial infarction. However, the limited view of 2-dimensional echocardiography reduces its ability to estimate perfusion abnormalities, especially in the subendocardial region. Three-dimensional echocardiography provides images of the left ventricular endocardium directly. This study was conducted to evaluate the ability of 3-dimensional MCE to assess abnormalities of subendocardial perfusion. Intracoronary 2- and 3-dimensional MCE was performed after primary percutaneous coronary intervention in 47 patients with acute myocardial infarction. Myocardial perfusion within the risk area was evaluated as good, poor, or no reflow on 2-dimensional MCE or as good, poor, or no myocardial opacification in endocardium on 3-dimensional MCE. The 2 methods showed different distributions of perfusion patterns: good, poor, and no reflow on 2-dimensional MCE in 31 (66%), 9 (19%), and 7 (15%) patients and good, poor, and no myocardial opacification in endocardium on 3-dimensional MCE in 17 (36%), 16 (34%), and 14 (20%) patients, respectively. Although only 19 patients (61%) with good reflow on 2-dimensional MCE showed myocardial perfusion grade 3 on angiography, 16 of 17 patients (94%) with good myocardial opacification in endocardium on 3-dimensional MCE showed myocardial perfusion grade 3. Although there were no significant differences in peak creatine kinase among the 3 subsets classified by 2-dimensional MCE, peak creatine kinase showed significant differences not only among the 3 groups but also among the subsets classified by 3-dimensional MCE. Classification by 3-dimensional MCE also predicted regional wall motion after 4.6 +/- 2.7 months, with significant differences between each pair of groups, whereas there was significant overlap of these values between the group with poor reflow and other 2 groups by 2-dimensional MCE. In conclusion, 3-dimensional MCE is a feasible way to assess subendocardial perfusion and predicts infarct size and functional recovery more precisely than 2-dimensional MCE.

Fatal case of amiodarone-induced acute respiratory distress syndrome in a patient with severe left ventricular dysfunction due to extensive anterior acute myocardial infarction.

We here report a case of 71-year-old man with acute extensive anterior myocardial infarction, who was complicated with ventricular tachycardia (VT) even after successful percutaneous coronary intervention. As intravenous administration of nifekalant terminated VT, we started oral administration of amiodarone (day 1). We gave 400 mg of amiodarone a day for the first week and 200 mg a day from the second week. The patient was stable with normoxia by day 20, in spite of pulmonary congestion-like infiltrates on chest X-ray. On day 21, he was complicated with acute respiratory distress syndrome. Immediate discontinuance of amiodarone and high-dose pulse glucocorticoid therapy with intubation slightly improved the infiltrations on chest X-ray. However, glucocorticoid therapy induced hyperglycemia with an increase in plasma osmolality, complicated with hypoalbuminemia, and gastrointestinal bleeding. Despite treatment with a large amount of saline, high-doses of catecholamines, and blood transfusion, the patient died on day 28. It is sometimes difficult to diagnose congestive heart failure or amiodarone-induced pulmonary infiltrates in patients with severe left ventricular dysfunction.