An Autopsy Case of Fulminant, Suppurative Bacterial Myocarditis Caused by Group B Streptococcus.

A 61-year-old woman was admitted to our hospital with a fever, nausea, diarrhea, and back pain. Her condition rapidly deteriorated, and she was transferred to the intensive-care unit for mechanical circulatory support and antibiotics, but she died 40 hours after admission. Autopsy findings showed necrotic and suppurative myocardial changes due to group B Streptococcus (GBS). To date, only one case of bacterial myocarditis caused by GBS has been reported. We herein report a case of GBS myocarditis, the etiology of which is poorly understood due to the limited number of cases. Bacterial myocarditis should be considered in patients with sepsis and myocardial dysfunction.

Abnormal P-wave terminal force in lead V1 is associated with cardiac death or hospitalization for heart failure in prior myocardial infarction.

The aim of this study was to clarify the prognostic significance of P-wave terminal force in lead V1 (PTFV1) in patients with prior myocardial infarction (MI). We retrospectively examined 185 patients with prior MI. The primary end point was cardiac death or hospitalization for heart failure. Abnormal PTFV1 was defined as PTFV1 ≥ 40 mm × ms. During a follow-up period of 6.4 ± 2.9 years, 39 patients developed the primary end point. A Kaplan-Meier analysis showed a lower primary event-free rate in 79 patients with abnormal PTFV1 than in 106 patients with normal PTFV1 (P < 0.001). When we classified 79 patients with abnormal PTFV1 into 31 with a purely negative P wave in lead V1 and 48 with a biphasic negative P wave in lead V1, the primary event-free rate did not differ between the two groups of patients. A multivariate Cox regression analysis selected age (hazard ratio (HR) 1.09, 95 % confidence interval (CI) 1.04-1.14, P < 0.001), multivessel coronary disease (HR 2.33, 95 % CI 1.02-5.28, P = 0.04), and abnormal PTFV1 (HR 2.72, 95 % CI 1.24-5.99, P = 0.01) as independent predictors of the primary end point. In conclusion, abnormal PTFV1 is an independent predictor of cardiac death or hospitalization for heart failure in patients with prior MI. The analysis of P waves in lead V1 should provide useful prognostic information in patients with prior MI.

Upright T waves in lead aVR are associated with cardiac death or hospitalization for heart failure in patients with a prior myocardial infarction.

The aim of the present study was to clarify the prognostic significance of upright T waves (amplitude > 0 mV) in lead aVR in patients with a prior myocardial infarction (MI). We retrospectively examined 167 patients with a prior MI. The primary end point was cardiac death or hospitalization for heart failure. During a follow-up period of 6.5 ± 2.8 years, 34 patients developed the primary end point. A Kaplan-Meier analysis showed a lower primary event-free rate in patients with upright T waves in lead aVR than in those with nonupright T waves in lead aVR (P = 0.001). Univariate Cox proportional hazards regression analyses showed that age, gender, chronic kidney disease, anterior wall MI, upright T waves in lead aVR, left ventricular ejection fraction, loop diuretic use, and spironolactone use were significantly associated with the primary end point. A multivariate Cox proportional hazards regression analysis selected age [hazard ratio (HR) 1.10, 95% confidence interval (CI) 1.05-1.16, P < 0.001], upright T waves in lead aVR (HR 3.10, 95% CI 1.23-7.82, P = 0.017), and loop diuretic use (HR 4.61, 95% CI 1.55-13.67, P = 0.006) as independent predictors of the primary end point. In conclusion, the presence of upright T waves in lead aVR is an independent predictor of cardiac death or hospitalization for heart failure in patients with a prior MI. The analysis of T-wave amplitude in lead aVR provides useful prognostic information in patients with a prior MI.

The number of leads with fragmented QRS is independently associated with cardiac death or hospitalization for heart failure in patients with prior myocardial infarction.

BACKGROUND: No information is currently available on the prognostic significance of the number of leads with fragmented QRS (fQRS). The objective of the study was to clarify the prognostic significance of the number of leads with fQRS in prior myocardial infarction (MI). METHODS AND RESULTS: We retrospectively examined 170 patients with prior MI. The primary end point was cardiac death or hospitalization for heart failure. During a mean follow-up period of 6.4 ± 2.9 years, 37 patients developed the primary end point. Univariate Cox proportional hazards regression analyses showed that age, male gender, chronic kidney disease, anterior wall MI, number of leads with fQRS, left ventricular ejection fraction, loop diuretic use, and spironolactone use were significantly associated with the primary end point. A multivariate Cox proportional hazards regression analysis selected age (hazard ratio [HR] 1.09, 95% confidence interval [CI] 1.04-1.14, p<0.001) and the number of leads with fQRS (HR 1.33, 95% CI 1.11-1.60, p=0.002) as predictors of the primary end point. A receiver operating characteristic curve analysis showed that the presence of ≥3 leads with fQRS was most useful for distinguishing between patients with and without the primary end point. A Kaplan-Meier analysis showed a lower primary event-free rate in patients with ≥3 leads with fQRS than in those with <3 leads with fQRS. CONCLUSIONS: The number of leads with fQRS, especially the presence of ≥3 leads with fQRS, is an independent predictor of cardiac death or hospitalization for heart failure in patients with prior MI.

A new electrocardiographic criterion to differentiate between Takotsubo cardiomyopathy and anterior wall ST-segment elevation acute myocardial infarction.

Several studies have examined the ability of electrocardiography to differentiate between takotsubo cardiomyopathy (TC) and anterior wall acute ST-segment elevation myocardial infarction (AA-STEMI). In those studies, the magnitude of ST-segment elevation was not measured at the J point. The American Heart Association, American College of Cardiology Foundation, and Heart Rhythm Society guidelines recommend that the magnitude of ST-segment elevation should be measured at the J point. Accordingly, the aim of this study was to retrospectively examine whether electrocardiography, using the magnitude of ST-segment elevation measured at the J point, could differentiate 62 patients with TC from 280 with AA-STEMI. Patients with AA-STEMI were divided into following subgroups: 140 with left anterior descending coronary artery occlusions proximal to the first diagonal branch (AA-STEMI-P), 120 with left anterior descending occlusions distal to the first diagonal branch and proximal to the second diagonal branch (AA-STEMI-M), and 20 with left anterior descending occlusions distal to the second diagonal branch (AA-STEMI-D). TC had a much lower prevalence of ST-segment elevation ≥1 mm in lead V(1) (19.4%) compared to AA-STEMI (80.4%, p <0.01), AA-STEMI-P (80.7%, p <0.01), AA-STEMI-M (80%, p <0.01), and AA-STEMI-D (80%, p <0.01). ST-segment elevation ≥1 mm in ≥1 of leads V(3) to V(5) without ST-segment elevation ≥1 mm in lead V(1) identified TC with sensitivity of 74.2% and specificity of 80.6%. Furthermore, this criterion could differentiate TC from each AA-STEMI subgroup, with similar diagnostic values. In conclusion, using the magnitude of ST-segment elevation measured at the J point, a new electrocardiographic criterion is proposed with an acceptable ability to differentiate TC from AA-STEMI.

ST-segment deviation in lead aVR on admission is not associated with left ventricular function at predischarge in first anterior wall ST-segment elevation acute myocardial infarction.

Previous studies have shown that the analysis of ST-segment deviation in lead aVR on admission provides useful information on angiographic coronary anatomy and risk stratification in acute coronary syndromes. However, the association between ST-segment deviation in lead aVR on admission and left ventricular (LV) function has not been fully investigated in anterior wall acute ST-segment elevation myocardial infarction. In this study, 237 patients with first anterior wall acute ST-segment elevation myocardial infarction were examined. The patients were divided into the following 3 groups according to ST-segment deviation in lead aVR on admission: 85 with ST-segment elevation ≥0.5 mm (group A), 106 without ST-segment deviation (group B), and 46 with ST-segment depression ≥0.5 mm (group C). LV ejection fractions at predischarge were compared among the 3 groups. Among the 3 groups, there were significant differences in the prevalences of proximal left anterior descending coronary artery (LAD) occlusion (group A 75.3%, group B 56.6%, group C 45.7%, p = 0.002), long LAD (group A 27.1%, group B 31.1%, group C 56.5%, p = 0.002), and good collaterals to the LAD (group A 40.0%, group B 25.4%, group C 17.4%, p = 0.01). LV ejection fractions at predischarge did not differ among the 3 groups (group A 56.4 ± 12.5%, group B 56.9 ± 12.7%, group C 53.3 ± 12.2%, p = 0.26). On a multiple regression analysis, establishment of Thrombolysis In Myocardial Infarction grade 3 flow, proximal LAD occlusion, and long LAD were associated with the LV ejection fraction at predischarge. In conclusion, ST-segment deviation in lead aVR on admission is not associated with LV function at predischarge in first anterior wall acute ST-segment elevation myocardial infarction.

Washout rate of cardiac iodine-123 metaiodobenzylguanidine is high in chronic heart failure patients with central sleep apnea.

BACKGROUND: The association between sleep-disordered breathing (SDB) assessed by polysomnography and cardiac sympathetic nerve activity (SNA) assessed by cardiac iodine-123 metaiodobenzylguanidine (123I-MIBG) imaging has not been investigated in patients with chronic heart failure (CHF). METHODS AND RESULTS: We performed cardiac 123I-MIBG scintigraphy and overnight polysomnography in 59 patients with stable CHF. The patients were classified into the 3 groups: 19 with no or mild SDB (NM-SDB, apnea-hypopnea index <15); 21 with central sleep apnea (CSA), and 19 with obstructive sleep apnea (OSA). The cardiac washout rate (WR) of 123I-MIBG was obtained from initial and delayed planar 123I-MIBG images. The WR was higher in patients with CSA (54.2 + or - 11.6%) than in those with OSA (37.9 + or - 8.6%, P < .05) or NM-SDB (40.8 + or - 8.8%, P < .05). The WR correlated positively with central apnea index (rho = 0.40, P = .002). A stepwise multiple regression analysis selected CSA and plasma brain natriuretic peptide levels as independent variables associated with the WR. CONCLUSIONS: The WR was higher in CHF patients with CSA than in those with OSA or NM-SDB, and CSA was independently associated with the WR, suggesting a link of CSA to increased cardiac SNA in CHF.

Significance of a prominent Q wave in lead negative aVR (-aVR) in acute anterior myocardial infarction.

PURPOSE: The aim of this study was to clarify the significance of a Q wave in lead negative aVR (-aVR) in anterior wall acute myocardial infarction (AMI). METHODS: Eighty-seven patients with a first anterior wall AMI were classified into 2 groups according to the presence (n = 17, group A) or absence (n = 70, group B) of a prominent Q wave (duration > or =20 milliseconds) in lead -aVR at predischarge. Group A had a higher prevalence of a long left anterior descending coronary artery (LAD), a lower left ventricular ejection fraction, and more reduced regional wall motion in the apical and inferior regions than group B. None of group A patients had an LAD that did not reach the apex. CONCLUSION: A prominent Q wave in lead -aVR in anterior wall AMI is related to severe regional wall motion abnormality in the apical and inferior regions, with an LAD wrapping around the apex.

Efficacy of single-bolus administration of sodium bicarbonate to prevent contrast-induced nephropathy in patients with mild renal insufficiency undergoing an elective coronary procedure.

We sought to clarify whether a single-bolus intravenous administration of sodium bicarbonate in addition to hydration with sodium chloride prevents contrast-induced nephropathy (CIN). One hundred forty-four patients with mild renal insufficiency (serum creatinine >1.1 to <2.0 mg/dl) undergoing an elective coronary procedure were randomly assigned to the following 2 groups: standard hydration with sodium chloride plus single-bolus intravenous administration of sodium bicarbonate (20 mEq) immediately before contrast exposure (group A, n = 72) and standard hydration alone (group B, n = 72). The primary end point was development of CIN, defined as an increase >25% or >0.5 mg/dl in serum creatinine within 3 days after the procedure. Incidence of the primary end point was lower in group A than in group B (1.4% vs 12.5%, p = 0.017). Incidence of adverse clinical events (acute pulmonary edema, acute renal failure requiring dialysis, and death within 7 days of procedure) did not differ between the 2 groups (0% vs 1.4%). In conclusion, single-bolus intravenous administration of sodium bicarbonate in addition to standard hydration can more effectively prevent CIN than standard hydration alone in patients with mild renal insufficiency undergoing an elective coronary procedure.

Electrocardiographic differentiation between occlusion of the first diagonal branch and occlusion of the left anterior descending coronary artery.

PURPOSE: We sought to electrocardiographically distinguish ST-segment elevation (STE)-acute myocardial infarction (AMI) caused by occlusion of the first diagonal branch (D1) from STE-AMI caused by occlusion of the left anterior descending coronary artery (LAD). METHODS: We examined 28 patients with STE-AMI caused by D1 occlusion (G-D) and 342 with STE-AMI caused by LAD occlusion (G-L). RESULTS: G-D had a higher prevalence of STE > or = 0.5 mm in each of leads I and aVL and a lower prevalence of STE > or = 1 mm in each of leads V(1) through V(6) than G-L. The prevalence of STE > or = 0.5 mm in lead aVL without STE > or = 1 mm in lead V(1) was higher in G-D (82.1%) than in G-L (9.4%, P < .01). CONCLUSION: ST-segment elevation > or = 0.5 mm in lead aVL without STE > or = 1 mm in lead V(1) may be useful to distinguish STE-AMI caused by occlusion of the D1 from STE-AMI caused by occlusion of the LAD.

Determinants of ST-segment level in lead aVR in anterior wall acute myocardial infarction with ST-segment elevation.

BACKGROUND: This study aimed to clarify the determinants of ST-segment level in lead aVR in anterior wall acute myocardial infarction (AAMI). METHODS: We analyzed ST-segment levels in all 12 leads on admission and emergency coronary angiographic findings in 261 patients with a first AAMI with ST-segment elevation. The length of the left anterior descending coronary artery (LAD) was classified as follows: short = not reaching the apex; medium = perfusing less than 25% of the inferior wall; long = perfusing 25% or more of the inferior wall. RESULTS: The ST-segment level in lead aVR correlated significantly with the ST-segment levels in leads I, II, III, aVF, V(1), and V(3-6), especially with those in leads II and V(6) (r = -0.63, P < .001; r = -0.61, P < .001; respectively). Patients with a proximal LAD occlusion had a greater ST-segment level in lead aVR than those with a distal LAD occlusion (P < .001). Patients with a long LAD had a lower ST-segment level than those with a short or medium LAD (P < .05). CONCLUSIONS: The ST-segment levels, especially in leads II and V(6), the site of the LAD occlusion, and the length of the LAD affect the ST-segment level in lead aVR in ST-segment elevation AAMI.

Comparison of sarpogrelate and ticlopidine in bare metal coronary stent implantation.

BACKGROUND: The efficacy and safety of sarpogrelate, a selective 5-hydroxytryptamine receptor subtype 2A antagonist, have not yet been established in bare metal coronary stenting. Accordingly, we sought to clarify whether treatment with sarpogrelate is clinically useful in bare metal coronary stenting. METHODS: A total of 450 patients who underwent successfully planned or unplanned bare metal coronary stenting were randomly divided into the following 2 groups: the sarpogrelate (300 mg/day) plus aspirin (100 mg/day) group (group S, n=225) and the ticlopidine (200 mg/day) plus aspirin (100 mg/day) group (group T, n=225). Either sarpogrelate or ticlopidine was administered for at least 4 weeks after the procedure. Follow-up coronary arteriography was performed at 6 months after the procedure. The primary endpoints were the incidence of adverse drug reactions requiring a withdrawal of treatment and the rate of binary restenosis. The secondary endpoint was the incidence of stent thrombosis. RESULTS: The incidence of adverse drug reactions requiring a withdrawal of treatment was significantly lower in group S than in group T (0.44% vs 8%, p=0.002). The rate of binary restenosis did not differ significantly between groups S and T (16.9% vs 18.2%). In addition, the incidence of subacute stent thrombosis did not differ between groups S and T (0.44% vs 0.44%). CONCLUSIONS: The incidence of adverse drug reactions requiring a withdrawal of treatment was significantly lower with sarpogrelate use than with ticlopidine use. The rate of binary restenosis and the incidence of subacute stent thrombosis did not differ between both drug groups.

Sinus arrest caused by occlusion of the sinus node artery during percutaneous coronary intervention for lesions of the proximal right coronary artery.

We examined the frequency of side-branch occlusion of the sinus node (SN) artery and of the subsequent sinus arrest in 80 consecutive patients who underwent percutaneous coronary intervention (PCI) for proximal right coronary artery (RCA) lesions. Side-branch occlusion of the SN artery occurred during PCI in 14 (17.5%) patients. Sinus arrest with junctional escape rhythm developed in 4 (28.6%) of these 14 patients. Temporary ventricular pacing was performed for one patient. The junctional escape rhythm disappeared in all of the patients within 3 days of the SN artery occlusion. The frequency of a single blood supply to the SN by the SN artery originating from the RCA did not differ significantly between the patients with and without sinus arrest (4/4 [100%]) vs 9/10 [90%]). In conclusion, although side-branch occlusion of the SN artery often occurs during PCI for proximal RCA lesions, where the SN artery originated, it does not always produce sinus arrest even in cases of a single blood supply to the SN by the SN artery originating from the RCA. Even though sinus arrest is caused by the occlusion of the SN artery, this bradyarrhythmia seems to disappear in the short term.

Relationship between beta-blocker treatment and the severity of central sleep apnea in chronic heart failure.

BACKGROUND: We sought to examine the relationship between use of beta-blockers and the severity of central sleep apnea (CSA) in patients with chronic heart failure. METHODS: We performed polysomnography in 45 patients with chronic heart failure (New York Heart Association functional class II/III and left ventricular ejection fraction < 50%) and examined the relationship between use of beta-blockers and the severity of CSA. Central apnea index (CAI) was used as an indicator of CSA. RESULTS: Patients receiving beta-blockers (ie, carvedilol; n = 27) had lower apnea-hypopnea index (AHI) and CAI than patients not receiving beta-blockers (n = 18) [mean +/- SD, 14 +/- 11 vs 33 +/- 17, p < 0.0001; and 1.9 +/- 3.2 vs 11 +/- 12, p = 0.0004, respectively]. AHI and CAI were negatively correlated with the dose of carvedilol (Spearman rho = - 0.61, p < 0.0001; and Spearman rho = - 0.57, p = 0.0002, respectively). Multiple regression analysis selected no use of beta-blockers as an independent factor of CAI (p = 0.0006). In five patients with CAI > 5 who underwent serial sleep studies, CAI decreased significantly after 6 months of treatment with carvedilol (9.5 +/- 4.9 to 1.3 +/- 2.4, p = 0.03). CONCLUSIONS: In patients with chronic heart failure, CAI was lower according to the dose of beta-blockers, and no use of beta-blockers was independently associated with CAI. In addition, 6 months of treatment with carvedilol decreased CAI. These results suggest that beta-blocker therapy may dose-dependently suppress CSA in patients with chronic heart failure.