Yoshiaki Sakai

Abnormal restitution property of action potential duration and conduction delay in Brugada syndrome: both repolarization and depolarization abnormalities

AIMS This study sought to examine the action potential duration restitution (APDR) property and conduction delay in Brugada syndrome (BrS) patients. A steeply sloped APDR curve and conduction delay are known to be important determinants for the occurrence of ventricular fibrillation (VF). METHODS AND RESULTS Endocardial monophasic action potential was obtained from 39 BrS patients and 9 control subjects using the contact electrode method. Maximum slopes of the APDR curve were obtained at both the right ventricular outflow tract (RVOT) and the right ventricular apex (RVA). The onset of activation delay (OAD) after premature stimulation was examined as a marker of conduction delay. Maximum slope of the APDR curve in BrS patients was significantly steeper than that in control subjects at both the RVOT and the RVA (0.77 +/- 0.21 vs. 058 +/- 0.14 at RVOT, P = 0.009; 0.98 +/- 0.23 vs. 0.62 +/- 0.16 at RVA, P = 0.001). The dispersion of maximum slope of the APDR curve between the RVOT and the RVA was also larger in BrS patients than in control subjects. The OAD was significantly longer in BrS patients than in control subjects from the RVOT to RVA and from the RVA to RVOT (from RVOT to RVA: 256 +/- 12 vs. 243 +/- 7 ms, P = 0.003; from RVA to RVOT: 252 +/- 11 vs. 241 +/- 9 ms, P = 0.01). CONCLUSIONS Abnormal APDR properties and conduction delay were observed in BrS patients. Both repolarization and depolarization abnormalities are thought to be related to the development of VF in BrS patients.

Prevalence and Clinical Features of Focal Takotsubo Cardiomyopathy

BACKGROUND Because it is difficult to distinguish between focal takotsubo cardiomyopathy and aborted myocardial infarction, there is little information about the prevalence and clinical features of focal takotsubo cardiomyopathy. METHODSANDRESULTS Our cardiac catheterization databases were queried to identify patients with focal takotsubo cardiomyopathy and other types of takotsubo cardiomyopathy. We defined focal takotsubo cardiomyopathy as hypo-, a- or dyskinesis in both anterolateral and septal segments without obstructive coronary artery disease explaining the wall motion abnormality. A total of 10 patients were diagnosed with focal takotsubo cardiomyopathy. The control group comprised patients with takotsubo cardiomyopathy with apical, mid-ventricular, or basal ballooning. Clinical features and in-hospital outcomes were compared between patients with focal takotsubo cardiomyopathy and those with other types of takotsubo cardiomyopathy. Among the 144 patients with takotsubo cardiomyopathy, the apical, mid-ventricular, basal, and focal types occurred in 85 (59.0%), 49 (34.0%), 0 (0%), and 10 patients (6.9%), respectively. The left ventricular ejection fraction was significantly higher in the focal group compared with the apical and mid-ventricular group (56±13 vs. 45±13 vs. 46±12%, P=0.03). In-hospital outcome was not significantly different among the 3 groups. CONCLUSIONS Focal takotsubo cardiomyopathy is not rare. Biplane left ventriculography is useful for its diagnosis. (Circ J 2016; 80: 1824-1829).

Transient focal left ventricular ballooning: a new variant of Takotsubo cardiomyopathy.

A 63-year-old woman suddenly felt chest pain after an argument. Since the symptom continued until the next day, she was taken to our hospital. The electrocardiogram showed significant ST-elevation in leads V2–4. Coronary angiography revealed no obstructive coronary artery disease. A left ventriculogram showed mid-anterior segmental ballooning associated with basal, mid-inferior and apical …

Recurrent mid-ventricular takotsubo cardiomyopathy

A 65-year-old woman was admitted for acute chest pain after choking on water. Coronary angiography revealed no obstructive coronary artery disease. Left ventriculogram demonstrated mid-ventricular akinesis with basal and apical hyperkinesis (Fig. 1a, b, video 1). The next day, cardiovascular magnetic resonance (CMR) imaging was performed. CMR demonstrated myocardial edema in the area of left ventricular wall motion abnormality (Fig. 1c) and no late gadolinium enhancement. Left ventricular ejection fraction by CMR was 52 % (video 2, 3). Echocardiogram on day 5 demonstrated complete recovery of the wall motion abnormality. Angiotensin II receptor blocker and statin were initiated during hospitalization, but discontinued due to an unspecified cause after discharge. Follow-up CMR at 5 months revealed no myocardial edema. Left ventricular ejection fraction was 72 %. Three years later, she presented with chest pain after choking on water that was the same trigger of the previous episode. Coronary angiography showed no obstructive coronary artery disease. Left ventriculogram demonstrated mid-ventricular akinesis that was nearly identical to the previous episode (Fig. 1d, e, video 4). CMR demonstrated myocardial edema (Fig. 1f) and no late gadolinium enhancement. Left ventricular ejection fraction was 54 % (video 5). She remained well after discharge with complete recovery of the wall motion abnormality. Repeated episode of mid-ventricular takotsubo cardiomyopathy is very rare. To our knowledge, this is the first report of recurrence of mid-ventricular takotsubo cardiomyopathy detected by serial left ventriculogram and cardiovascular magnetic resonance imaging.

Mid-ventricular takotsubo cardiomyopathy preceding acute myocardial infarction

A 71-year-old woman with a history of hypertension suddenly felt chest pain after an argument with her family. Because the symptom completely subsided an hour later, she did not consult any physician at that time. Two days later she felt chest pain again and was taken to our hospital. The electrocardiogram showed ST-elevation in leads II, III, and aVF and negative T waves with QT prolongation in leads I, aVL, and V3–6. Coronary angiography revealed total occlusion of a septal branch of the distal left anterior descending coronary artery (Fig. 1a). Left ventriculogram demonstrated mid-ventricular akinesis with preserved basal and apical wall motion (Fig. 1b). Troponin I level was 1.332 pg/mL on admission and creatine kinase was elevated to 550 U/L 12 h after admission. On day 3, cardiovascular magnetic resonance (CMR) imaging demonstrated regional myocardial edema in the area matched to the distribution of wall motion abnormality (Fig. 1c) and late gadolinium enhancement in the territory of the obstructed coronary artery (Fig. 1d). Echocardiogram on day 6 demonstrated improvement of global LV ejection fraction. Five months later follow-up CMR revealed complete recovery of the wall motion abnormality except the infarcted area (Fig. 1e). Diagnosis of takotsubo cardiomyopathy requires the absence of obstructive coronary disease [1]. Therefore, when obstructive coronary disease coexists, accurate diagnosis of takotsubo cardiomyopathy is difficult and such cases may be misdiagnosed as acute coronary syndrome. In the present case, pathological assessment of myocardium by CMR led us to proper diagnosis. When the area of wall motion abnormality is not identical to the territory of obstructed vessel, one should suspect coexistence of takotsubo cardiomyopathy with obstructive coronary disease and CMR must be checked. In the present case, it is unclear whether preceding mid-ventricular takotsubo cardiomyopathy was associated with the subsequent development of acute myocardial infarction. However, it might be possible that mechanical stress around the distal hinge point of anterior wall produced intimal injury of nearby small coronary arteries, which resulted in acute thrombosis. Some researchers have reported the case of takotsubo cardiomyopathy secondary to acute myocardial infarction [2], however, to the best of our knowledge, this is the first case of mid-ventricular takotsubo cardiomyopathy preceding acute myocardial infarction.

Impact of tissue protrusion after coronary stenting in patients with ST-segment elevation myocardial infarction

Clinical impact of tissue protrusion (TP) after coronary stenting is still controversial, especially in patients with ST-segment elevation myocardial infarction (STEMI). A total of 104 STEMI patients without previous MI who underwent primary percutaneous coronary intervention (PCI) under intravascular ultrasound (IVUS)-guidance were included. Post-stenting grayscale IVUS analysis was performed, and the patients were classified according to the presence or absence of post-stenting TP on IVUS. Coronary angiography and single-photon emission computed tomography myocardial perfusion imaging (SPECT MPI) with 99mTc tetrofosmin were analyzed. Major adverse cardiac events were defined as cardiovascular death, myocardial infarction, heart failure hospitalization, and target vessel revascularization. TP on IVUS was detected in 62 patients (60%). Post-PCI coronary flow was more impaired, and peak creatine kinase-myoglobin binding level was higher in patients with TP compared to those without. SPECT MPI was performed in 77 out of 104 patients (74%) at 35.4 ± 7.7 days after primary PCI. In patients with TP, left ventricular ejection fraction was significantly reduced (47.5 ± 12.0% vs. 57.6 ± 11.2%, p < 0.001), and infarct size was larger [17% (8–25) vs. 4% (0–14), p = 0.002] on SPECT MPI. During a median follow-up of 14 months after primary PCI, Kaplan–Meier analysis demonstrated a significantly higher incidence of major adverse cardiac events in patients with TP compared to those without. TP on IVUS after coronary stenting was associated with poor outcomes in patients with STEMI.

Reply: Takotsubo syndrome-induced acute myocardial infarction

We thank Dr. Madias for his valuable comments on our case report, published online on February 22, 2015 ahead of print in the journal [1]. We would like to respond to his important question about transient attenuation of the voltage of the QRS complexes (AVQRS). During the acute phase, QRS complexes in leads I and aVL were 4.5 and 1 mm in amplitude, respectively, under the presence of myocardial edema detected by cardiac magnetic resonance imaging. Five months later QRS complexes in leads I and aVL have been amplified to 6.5 and 2 mm, respectively, corresponding to the complete recovery of wall motion abnormality except infarcted area. In the present case, mid-ventricular takotsubo cardiomyopathy preceded acute myocardial infarction (AMI). The amplitudes of QRS complexes in leads I and aVL have not been affected by subsequent AMI, because we observed significant ST elevation in leads II, III and aVF on admission as an electrocardiographic change associated with AMI. Therefore, we assume that transient AVQRS in leads I and aVL was possibly caused by mid-ventricular takotsubo cardiomyopathy as suggested by Dr. Madias.