Reliability of ST-segment shifts in the synthesized V3R-V5R leads after coronary balloon inflations during percutaneous coronary intervention.

Obtaining a right-chest electrocardiogram is essential for diagnosing concomitant right ventricular infarction in patients with inferior wall acute myocardial infarctions. A software program to synthesize right-chest electrocardiographic waveforms from 12-lead electrocardiographic waveforms is available in Japan. However, its reliability has not been fully investigated. Accordingly, the aim of this study was to examine the reliability of ST-segment shifts in the synthesized V3R to V5R leads. ST-segment shifts in actual and synthesized V3R to V5R leads were compared during the last 10 seconds of 131 balloon inflations while performing elective percutaneous coronary intervention in 56 patients with coronary artery disease. ST-segment shifts in the actual and synthesized V3R, V4R, and V5R leads were correlated (r = 0.96, p <0.001, r = 0.94, p <0.001, and r = 0.91, p <0.001, respectively). A Bland-Altman analysis showed that the bias between ST-segment shifts in the actual and synthesized V3R to V5R leads was -3.1, -5.4, and -4.2 µV, respectively, while the limits of agreement between the ST-segment shifts in the actual and synthesized V3R to V5R leads were -59.2 to 52.9, -61.9 to 51.1, and -59.7 to 51.3 µV, respectively. The κ coefficients for ST-segment elevation of ≥50 and ≥100 µV in the actual and synthesized V3R, V4R, and V5R leads were 0.83 and 0.81, 0.66 and 0.83, and 0.57 and 0.80, respectively. In conclusion, these results indicate that ST-segment shifts in the synthesized V3R to V5R leads have acceptable reliability, suggesting that synthesized right-chest electrocardiography can be used to diagnose concomitant right ventricular infarction in patients with inferior wall acute myocardial infarctions.

Takotsubo cardiomyopathy triggered by lateral wall ST-segment elevation myocardial infarction.

We herein report the case of a 72-year-old female with a lateral wall acute myocardial infarction (MI) complicated by takotsubo cardiomyopathy (TC). The patient presented with "severe" chest pain lasting for one hour. She did not experience any obvious emotional or physical stress preceding the chest pain. An admission electrocardiogram showed ST-segment elevation in leads I, aVL, and V6 and ST-segment depression in leads II, III, aVF, and V1. Emergent coronary angiography showed total occlusion of the obtuse marginal branch. Subsequently, primary percutaneous old balloon angioplasty followed by everolimus-eluting stenting was performed. Left ventriculography performed immediately after final coronary angiography revealed hypokinesis in the lateral wall and mid-ventricular ballooning. The electrocardiographic findings and left ventricular wall motion later normalized. Cardiac magnetic resonance imaging showed late gadolinium enhancement in the lateral wall. In conclusion, to the best of our knowledge, this is the second case report of TC triggered by an acute MI, which provides further evidence that an acute MI can potentially trigger TC. .

Gender differences in symptoms during 60-second balloon occlusion of the coronary artery.

Previous investigations have demonstrated the presence of gender differences in the symptoms of angina pectoris and acute coronary syndrome. However, most of these investigations have had certain limitations, including being retrospective, an interview-related bias, a various duration of myocardial ischemia, and a lack of multivariate analysis, all of which would have affected the results. Accordingly, we prospectively examined the presence or absence of chest pain and non-chest pain symptoms during a 60-second balloon inflation in the setting of percutaneous coronary intervention, which provides a unique model of transient myocardial ischemia, in 110 men and 80 women with coronary artery disease. Chest pain and/or non-chest pain symptoms (occipital pain, jaw pain, neck/throat pain, shoulder pain, upper arm pain, back pain, and nausea) were observed during the balloon inflation in 72 men and 52 women. In the 124 patients with any symptoms during the balloon inflation, non-chest pain symptoms were more common in women than in men (31% vs 14%, p = 0.02); however, the incidence of chest pain did not differ between the men and women. After adjustment for covariables, including age, body mass index, hypertension, diabetes mellitus, current smoking, previous myocardial infarction, target vessels, ß-blocker use, and calcium antagonist use, female gender remained significantly associated with non-chest pain symptoms (odds ratio 3.3, 95% confidence interval 1.2 to 9.9, p = 0.02). In conclusion, non-chest pain symptoms during the 60-second balloon occlusion of the coronary artery were more common in women than in men, supporting the presence of the gender difference in myocardial ischemic symptoms.

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.

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.

Plasma homocysteine level is unrelated to long-term cardiovascular events in patients with previous percutaneous coronary intervention.

OBJECTIVES: It is unclear whether plasma homocysteine (Hcy) level affects long-term outcomes in patients with previous percutaneous coronary intervention (PCI). Accordingly, we investigated the association of plasma Hcy level with long-term major adverse cardiovascular events (MACEs), especially with recurrence of angina pectoris (AP) or new myocardial infarction (MI) in patients with previous PCI. METHODS: A total of 231 patients with previous (>12 months) PCI were followed up for a median period of 49 months. The primary end point was recurrence of AP or new MI. The secondary end points were MACEs (cardiovascular death, recurrence of AP, new MI, revascularization therapy, hospitalization for heart failure, or stroke). RESULTS: During the follow-up period, 35 patients (15.2%) had a primary end point, and 58 (25.1%) had a secondary end point. A univariate analysis by a Cox proportional hazards regression model showed that plasma Hcy level was not associated with the primary (hazard ratio [HR] 1.13, 95% confidence interval [CI] 0.41-3.08, p=0.82) and secondary (HR 1.60, 95% CI 0.75-3.42, p=0.23) end points. The adjustment for other clinical variables did not alter the results. CONCLUSIONS: Plasma Hcy level appears to be unrelated to recurrent AP, new MI, and long-term MACE within coronary artery disease patients with previous PCI.

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.