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Takotsubo syndrome (TTS) is a transient cardiomyopathy that is often associated with cerebrovascular diseases. Earlier studies have supported the concept that the cardiovascular system is regulated by a central autonomic network (CAN) consisting of the insular cortex (IC), anterior cingulate gyrus and amygdala. We report the case of a 79‐year‐old female diagnosed with a mid‐ventricular variant of TTS concomitant with right IC ischaemic stroke. After 12 h of hospitalization, she experienced a sudden collapse. Rapid cardiopulmonary resuscitation resulted in a return of spontaneous circulation. Subsequent left ventriculography revealed akinesis in the mid‐portion of the left ventricle with vigorous contraction of the basal and apex segment. Two weeks after admission, cardiac ultrasound showed improved left ventricular contraction. Right IC ischaemia in this patient might have been associated with a dysregulation of the CAN and subsequent increased sympathetic nervous system activity that triggered TTS.

Although short and long sleep duration are both risk factors of cardiovascular disease (CVD), the recent meta‐analyses have been shown that long sleep duration was closely associated with CVD mortality. While the specific mechanism underlying the association between long sleep duration and CVD remains unclear, long sleep duration was shown to be associated with arterial stiffness and blood pressure variability (BPV) in many Asian populations. This review article will focus on the pathophysiology of long sleep duration, arterial stiffness, BPV and their effects on CVD. To set the stage for this review, we first summarize the current insights for the relationship between long sleep duration and CVD in relation to arterial stiffness and BPV.

Earlier studies have shown that visit-to-visit blood pressure (BP) variability (VVV) served as a significant independent risk factor of stroke, specifically, in the high-risk elderly of cardiovascular disease (CVD). Although the mechanism is not clearly understood, arterial remodeling such as carotid artery, coronary artery and large aortic artery would be a strong moderator in the relationship between VVV and CVD incidence. Recent studies have provided evidence that VVV predicted the progression of arterial stiffness. While the class of antihypertensive agents is suggested to be an important determinant of VVV, long-acting calcium channel blockers use (CCBs) is associated with the reduction of VVV, and thus, is suggested to decrease the arterial stiffness. Specifically, the relationship between VVV and coronary arterial remodeling has never been reviewed until now. This article summarizes the recent literature on these topics. In the elderly hypertensives, strict BP control using CCBs could play a pivotal role in suppressing arterial stiffening via VVV reduction.

Funding Acknowledgements Type of funding sources: None. Background Thrombus in left atrial appendage (LAA) is associated with cardiogenic ischemic stroke, and anticoagulation therapy is utilized to prevent thromboembolism. Purpose This study is to investigate the incidence of thrombus in left atrial appendage detected by transoesophageal echocardiography (TOE) under anticoagulation therapy with warfarin or direct oral anticoagulants (DOAC). Methods Between 2005 and 2016, the patients who underwent TOE under anticoagulation therapy due to atrial fibrillation more than one month were enrolled in this study. The patients were divided into 2 groups according to whether treated with warfarin or DOAC and baseline characteristics and incidence of LAA thrombus were assessed. Results Among the 313 study patients, 243 (78%) were treated with warfarin. The patients treated with warfarin were elder (median 73 y vs. 67 y [interquartile range 66 – 78 y vs. 58 – 72 y], P < 0.01), the body mass index was lower (23.2 vs. 24.0 [21.0 – 25.4 vs. 21.3 – 26.9], P = 0.03). The prevalence of male sex (64% vs. 71%, P = 0.26) were similar between the 2 groups. The previous history of hypertension (69% vs. 59%, P = 0.10), diabetes (24% vs. 19%, P = 0.32), vascular disease (30% vs. 26%, P = 0.52), and ischemic stroke were similar between the 2 groups (30% vs. 23%, P = 0.22). The prevalence of CHA2DS2-VASc score > 1 (84% vs. 59%, P < 0.01) and the d-dimer level (0.7 vs. 0.5 mcg/ml [0.5 – 1.8 vs. 0.5 – 0.5 mcg/ml], P < 0.01) were higher in the warfarin groups than those of the DOAC. The velocity of LAA was slower in the warfarin group than those of DOAC (35 vs. 55 cm/s [21 – 54 vs. 38 – 68 cm/s], P < 0.01). The incidence of detection of LAA thrombus was 19% in the warfarin group and 3% in the DOAC group (P < 0.01). In the warfarin group, the PT-INR were lower in the patients with LAA thrombus (1.38 vs. 1.66 [1.11 – 1.92 vs. 1.34 – 2.03], P = 0.03). Conclusions The higher risk of ischemic stroke and out of range PT-INR may be the cause of the higher incidence of LAA thrombus in the patients treated with warfarin than those with DOAC. Abstract Figure.

Introduction: Idiopathic ventricular fibrillation (IVF) including Brugada syndrome (BS) is one of causes of cardiac arrest without prior overt cardiac dysfunction. Hypothesis: We assessed the hypothesis that patents of IVF had favor outcomes than those of non-IVF after cardiac arrest treated with targeted temperature management (TTM). Methods: Patients who were treated with TTM after cardiac arrest between 2000 and 2019 were enrolled in the study. Patients were divided into 2 groups according to whether the patients were diagnosed as IVF or not. The patients treated with TTM were routinely performed coronary angiography. Results: Among the study patients (N = 306), 35 (11%) patients were IVF and 7 were BS. The patients of the IVF group were significantly younger (median 53 y vs. 64 y) than those of the non-IVF group. The prevalence of initial rhythm was shockable (69% vs. 47%, P = 0.02) was significantly higher in the patients of the IVF group than those of the non-IVF group. Among the patients in the non-IVF group, 114 patients (42%) were diagnosed as acute coronary syndrome and 93 patients (35%) were treated with coronary revascularization. The prevalence of male sex (77% vs 74%, P = 0.70) and witnessed to arrest (80% vs. 81%, P = 0.87), and low-flow time (29 min vs. 38 min [20 - 43 min vs. 21 - 52 min, P = 0.15]) were similar between the 2 groups. The prevalence of performing extracorporeal resuscitation (9% s 43%, P < 0.001) were lower in the patients of the IVF group. The 8-y survival rate were shown in the figure. All of the BS patients were witnessed arrest and were discharged without severe neurological deficit. The IVF as the cause of arrest was independently associated with 8-y survival. Conclusions: The patients of IVF had favor outcomes than those of non-VF. One of causes may be the lower prevalence of requiring extracorporeal circulatory support due to less cardiac dysfunction. The patients of BS had the tendency toward higher survival rate than those of non-BS IVF patients.

Introduction: Mortality in patients with acute coronary syndrome (ACS) due to unprotected left main coronary artery (LMA) occlusion is high. Extracorporeal membrane oxygenation (ECMO) could rapidly provide circulatory support. Hypothesis: This study aimed to verify the hypotheses that the patient who required circulatory support with ECMO in acute phase of LMA-ACS had greater cardiac function deterioration and had higher mortality in the chronic phase than those who did not require ECMO. Methods: Patients with LMA-ACS who underwent percutaneous coronary revascularization between 2000 and 2020 were enrolled in this study. The patients were divided into two groups based on whether or not they received ECMO. Thirty-day (acute phase) and 30-day to 6-year (chronic phase) survival curves were constructed by Kaplan-Meier method. The cause of death in acute and chronic phase were examined. Results: Among the 85 study patients, 23 (27%) were in the ECMO-group. Median age was younger in the ECMO-group (65 y [57 - 72] vs. 73 y [69 - 83], p < 0.01), and male sex (67% vs. 63%) were similar in ECMO group and non-ECMO groups respectively. The prevalence of ST elevation myocardial infarction (STEMI), non-STEMI, unstable angina were 52%, 48%, and 0% vs. 15%, 42%, and 44% in the ECMO group and non-ECMO group, respectively. The 30-day mortality was significantly higher in ECMO group (61% vs. 15%, p < 0.01); however, the 30-day to 6-year mortality was similar between the two groups (41% vs. 33%, p = 0.59) (Figure). The cause of death in the acute phase were cardiac failure (79% and 67%) and those in chronic phase were cardiac failure (50% and 25%), malignancy (0% and 13%), and infection (50% and 36%). Conclusions: The mortality in chronic phase in LMA-ACS patients who survived up to 30 days were similar in ECMO group and non-ECMO group. Moreover the patients whose cardiac function deteriorated severely and required ECMO in acute phase had similar prognosis to those that did not require ECMO.

Introduction: While clinical predictors of plaque erosion (PE) in patients with acute coronary syndromes (ACS) were reported, PE was more frequently observed in the population with normal kidney function. On the other hand, earlier studies indicated that spotty calcification related to plaque rupture on the culprit site in ACS. However, the morphological features of coronary calcification on culprit site have not been investigated in relation to PE. Hypothesis: We assessed the hypothesis that the morphology of calcification on culprit site was associated with PE in ACS patients without chronic kidney disease (CKD). Methods: In the 166 ACS patients (66.9±10.7 years old, male 83 %), based on Optical Coherence Tomography/ Optical Frequency Domain Imaging, existence of PE on culprit site was investigated. In the morphological features of coronary calcification, the maximum thickness, maximum area, maximum angle, minimum depth from the lumen in axial sections, and the length in longitudinal image were determined. Results: There were the 73 patients with PE, 58 patients with calcification and 38 patients with CKD. A marginal significant difference in thickness (300 vs 190μm, p=0.07) and significant difference in angle (60 vs 23degree, p=0.001), area (0.89 vs 0.43mm 2 , p=0.001) and length (2.34 vs 1.12 mm, p=0.03) were observed between the patients with PE and the patients without PE. In the multiple regression analysis adjustment for age, gender, region location, maximum creatine phosphokinase, STEMI or not, diabetes mellitus, angiotensin receptor blockers use, statin use and systolic blood pressure on admission, angle (OR: 1.01, 95%CI: 1.002 to 1.013, p=0.005) and area (OR: 1.46, 95%CI: 1.02 to 2.1, p=0.04) each had significant associations with PE. Specifically, only in the patients without CKD, thickness (p=0.025), angle (p=0.003) and area (p=0.013) were significant indicators of PE. Conclusions: In conclusion, morphology of calcification on culprit site was a significant indicator of PE in the patients with ACS. Specifically, larger calcification might serve as a pathophysiology underlying in the phenotype of plaque vulnerability in ACS patients with normal kidney function.

Background Thrombus in left atrial appendage (LAA) is associated with cardiogenic ischemic stroke; however, little is known about prognosis of patients with LAA thrombus detected by transoesophageal echocardiography (TOE). Purpose This study is to investigate the prognosis of patients with LAA thrombus and their cause of death. Methods Between 2005 and 2016, the patients who were performed TOE in our hospital were enrolled in this retrospective observational study. Five-year stroke free and survival curves were constructed by Kaplan-Meir method and cause of death were assessed. Results Among the 1263 study patients, LAA thrombus was detected in 146 (12%) patients. The patients with LAA thrombus were elder (74 y [66–79 y] vs. 70 y [62–76 y], P Conclusions The patients who were detected thrombus in the LAA had higher incidence of ischemic stroke; however, the 5-y survival were similar. The ischemic stroke was not major cause of death in the patients with and without LAA thrombus. The higher rate of receiving anticoagulation therapy may be one of the causes of the discrepancy. Figure 1 Funding Acknowledgement Type of funding source: None

Background Regardless of patients’ baseline renal function, worsening renal function (WRF) during hospitalization is associated with poor outcomes. In individuals with acute heart failure (AHF), one predictor of WRF is an early drop in systolic blood pressure (SBP). Few studies have investigated WRF in elderly AHF patients or the influence of these patients’ heart rate (HR) at admission on the relationship between an early SBP drop SBP and the AHF. Methods We measured the SBP and HR of 245 elderly AHF inpatients (83 ± 6.0 years old, females 51%) at admission and another six times over the next 48 h. We defined ‘WRF’ as a serum creatinine increase ≥0.3 mg/dL by Day 5 post-admission. We calculated the ‘early SBP drop’ as the difference between the admission SBP value and the lowest value during the first 48 h of hospitalization. Results There were significant differences between the 36 patients with WRF and the 209 patients without WRF: early SBP drop (51 vs. 33 mmHg, p p p p Conclusions In these elderly AHF patients, exaggerated early SBP drop and lower HR at admission were significant independent predictors of WRF, and these factors were additively associated with WRF.

Background Left atrial appendage (LAA) thrombus is one of causes of cardiogenic stroke and detection of LAA thrombus by transoesophageal echocardiography (TOE) strongly suggest cardiogenic stroke. It was reported that cardiogenic stroke patients had higher in-hospital mortality about 19%; however, little is known about LAA thrombus and mortality after indexed detection of LAA thrombus. We investigated LAA thrombus detection and their prognosis including ischemic stroke and survival. Methods The patients who were performed TOE between 2005 and 2016 in our hospital were enrolled in this study. Patients were divided into 2 groups based on thrombus detection in the LAA, and baseline characteristics and outcomes including prevalence of 5-y stroke-free and survival from the indexed TOE were compared. Results Among the 1260 study patients, the follow-up duration was median 971 d (interquartile range 345 d – 2017 d), and 67% of the patients were performing TOE for atrial fibrillation (AF), 20% for cerebral infarction, and 14% for valvular heart disease. Non-valvular AF was seen in 64% of the study patients and rheumatic AF was in 2%. The age (74 y [66 y – 79 y] vs 70 y [62 y – 76 y], p < 0.001), the prevalence of male sex (67% vs 69%, p = 0.63), and hemoglobin level (13.9 g/dl [12.5 – 15.1 g/dl] vs 13.8 g/dl [12.4 – 14.9 g/dl], p = 0.49) were similar between the patients with LAA thrombus and those without. The CHA2DS2-VASc score (p = 0.008), the prevalence of receiving anticoagulation before TOA (34% vs 24%, p = 0.01), those of after TOA (98% vs 66%, p < 0.001), serum creatinine (0.92 mg/dl [0.80 – 1.10 mg/dl] vs 0.85 mg/dl [0.71 – 1.00 mg/dl], p < 0.001), d-dimer level (1.7 mcg/ml [0.9 – 3.5 mcg/ml] vs 0.8 mcg/ml [0.5 – 2.2 mcg/ml], p < 0.001), and plasma brain natriuretic peptide (315 pg/ml [128 – 515 pg/ml] vs 126 pg/ml [47 – 284 pg/ml], p < 0.001) were higher in the patients with LAA thrombus than those without. The 5-y ischemic stroke-free rate was lower in the patients with LAA thrombus than those without (p < 0.001) (Figure, Panel A); however, the 5-y survival was similar between the 2 groups (p = 0.93) (Panel B). Conclusions The patients who were detected thrombus in the LAA had higher incidence of ischemic stroke, but the survival rate were similar. The higher rate of receiving anticoagulation therapy in the patients with LAA thrombus may be the cause of this discrepancy. Further studies are necessary to clarify this issue. Abstract P765 Figure

Introduction Paradoxical cerebral infarction is a mechanism of acute ischemic stroke; however, definitive images to diagnose paradoxical embolism are not often obtained. We report a case of paradoxical cerebral embolism complicated with cardiac arrest due to massive pulmonary embolism. Case report A 40-year-old man presented due to sudden-onset chest pain, and was admitted to our hospital. He was restless and had cold sweat; we could not measure blood pressure. Electrocardiography showed wide QRS complex with right bundle branch block, and T wave inversion in leads V1 and III. Transthoracic echocardiography showed diffuse severe left ventricular hypokinesis, with slightly better inferior wall motion compared to other segments. Few minutes after arriving, he experienced cardiac arrest; chest compression was initiated. He was transported to the catheter laboratory, and veno-arterial extracorporeal membrane oxygenation was initiated subsequently. To diagnose the cause of arrest, we performed coronary angiography, which revealed no occluded coronary artery. Pulmonary angiograms showed bilateral proximal pulmonary artery occlusion with massive thrombi (panel A). Surgical embolectomy was performed after cardiac team discussion. After ICU admission post-surgery, pericardial effusion was increased, and the blood drained continuously from the chest tube; a large amount of blood transfusion was required. Reopen chest haemostasis was utilised. After the second ICU admission, anisocoria was observed; subsequent computed tomography showed low density and midline shift in almost the entire left cerebral hemisphere (Panel B). Carotid duplex ultrasound revealed a large thrombus saddled at the left carotid artery bifurcation (Panel C and D). We rechecked the transthoracic echocardiogram at arrival to reveal the cause of the cerebral infarction, which showed the thrombus to be at the ascending aorta (Panel E). We thought that the thrombi had moved from the lower limb to the right atrium. The massive pulmonary embolism increased the pulmonary artery and right atrial pressure, resulting in the lower pressure of the left atrium compared to that of the right atrium. The thrombi passed through the patent foramen ovale into the left atrium, moved into the left ventricle, and embolised the left internal carotid artery (Panel F). He expired due to severe neurologic injury from brain herniation. Conclusion In this case, although the pulmonary embolism was massive and led to cardiac arrest, the deteriorated haemodynamics improved by extracorporeal cardiopulmonary resuscitation and surgical embolectomy. However, we could not rescue the patient because of the severe neurological injury due to paradoxical embolism. Paradoxical cerebral infarction in pulmonary embolism is rare; however, we should pay careful attention to early detection of paradoxical cerebral infarction in pulmonary embolism and treatment for return of the patient to the former lifestyle. Abstract P684 figure

Transient left ventricular dysfunction in patients under emotional stress, also known as Takotsubo cardiomyopathy, has been recognized as a distinct clinical entity. Recent studies have supported the concept notion that the cardiovascular system is regulated by cortical modulation. A network consisting of the insular cortex (Ic), anterior cingulate gyrus, and amygdala plays a crucial role in the regulation of the central autonomic nervous system in relation to emotional stress such as anxiety, fear and sadness. Because the Ic is located in the region of the middle cerebral arteries, its structure tends to be exposed to a higher risk of cerebrovascular disease. Ic damage has been associated with myocardial injury, increased brain natriuretic peptide, and the incidence of Takotsubo cardiomyopathy. Because Ic damage has been associated with increased sympathetic nervous system activity, Ic damage is suggested to have a pivotal role in the pathophysiology of Takotsubo cardiomyopathy. In this review, we focus on the role of the Ic as a mediator for the cardiovascular system in relation to emotional stress, and we summarizes the current knowledge on the relationships between the Ic and Takotsubo cardiomyopathy.

The cardiovascular system is regulated by a central autonomic network (CAN) consisting of the insular cortex, anterior cingulate gyrus, and amygdala. Because the insular cortex often tends to be damaged in patients with herpes simplex virus (HSV) encephalitis, the autonomic instability observed in these patients was suggested to be moderated by an insular cortex lesion. Here, we report the case of a 51-year-old Japanese male who was hospitalized following a collapse 5 days earlier; he was diagnosed as herpes encephalitis. Diffusion-weighted MRI revealed asymmetric right greater hyperintensity throughout his insular cortex and anterior cingulate gyrus. At 1 week after admission, transthoracic echo showed diffuse hypokinesis in the left ventricle (LV). Cardiac 123I-meta-iodobenzylguanidine uptake (123I-MIBG) scintigraphy revealed reduced uptake in the inferior and posterior wall. Electrocardiograhy at rest showed that the coefficient variation of RR intervals (CVR-R) was reduced, and the corrected QT (QTc) interval length was prolonged. In this HSV encephalitis patient, signs of a right insular cortex lesion and autonomic instability were observed: LV hypokinesis, regional reduced 123I-MIBG uptake, decreased CVR-R, and QTc interval prolongation. Our patient’s autonomic instability may thus be derived from disrupted autonomic balance due to the right insular cortex lesion.

Background Renal dysfunction is a frequent finding in patients hospitalized for acute heart failure (AHF). Worsening renal function (WRF) during hospitalization was found to be related with a poor outcome independently of baseline renal function. Early drop in systolic blood pressure (SBP) has shown to predict WRF in AHF. However, there have been few studies that reported the impact of on-admission heart rate (HR) on the relationship between early SBP drop and WRF in the elderly AHF. Purpose We assessed the hypothesis that early SBP drop predict WRF in the elderly patients with AHF, and investigated that on-admission HR might have an interaction with that relationship. Methods SBP and HR were measured on admission and 6 times during 48 hours in the 245 elderly AHF inpatients (82.9±6.0 years old, male 49.4%). WRF was defined as a serum creatinine increase of ≥0.3 mg/dL by Day 5. Early drop in SBP was calculated as the difference between admission and the lowest value measured during the first 48 hour of hospitalization. Results Early SBP drop (51.3 vs 32.5mmHg, p Conclusions In the elderly AHF patients, exaggerated early SBP drop and lower on-admission HR were shown as significant independent predictors of WRF. These two factors were additively associated with WRF. Too much reduction in SBP and that in HR might be harmful to renal circulation in AHF.

Visit-to-visit blood pressure variability has been shown to be an independent risk factor for stroke and cognitive impairment. However, the underlying mechanisms are not fully understood. Artery remodeling and silent cerebral injury are suggested to be involved in the relationship between visit-to-visit blood pressure variability and cognitive impairment. The present review article summarizes the recent literature on these topics. Here we review visit-to-visit blood pressure variability, artery remodeling, silent cerebral injury and an issue regarding the impact of these components on dementia including Alzheimer's disease.

Left atrial appendage (LAA) thrombus is one of causes of cardiogenic stroke and detection of LAA thrombus by transesophageal echocardiography (TEE) strongly suggest cardiogenic stroke; however, little is known about detection of LAA thrombus and long-term prognosis. We investigated LAA thrombus

The Takotsubo cardiomyopathy is often considered autochthonous to the heart, although the primary problem may be not in the heart muscle itself. Instead, similar to several Takotsubo‐like cardiac pathologies seen in acute neurological diseases, it may reflect the capacity of the nervous system to injure the heart. Persuasive evidence exists that shocking emotional stress promotes direct heart injuries. Moreover, clinical and laboratory research shows that cardiac structural damage can occur in the presence of a normal heart, especially in the context of seizures, stroke, and traumatic brain injury or under conditions of psychological stress. The aim of this review is to summarize the clinical implications of these observations, several of which focus on the pivotal role of the insula of Reil in the brain‐heart connection, to unravel the mystery of Takotsubo cardiomyopathy pathogenesis.

Background: The CHADS2 scoring system is simple and widely accepted for predicting thromboembolism in patients with nonvalvular atrial fibrillation (NVAF). Although congestive heart failure (CHF) is a component of the CHADS2 score, the definition of CHF remains unclear. We previously reported that the presence of CHF was a strong predictor of left atrial appendage (LAA) thrombus. Therefore, the present study aimed to elucidate the relationship between LAA thrombus and the brain natriuretic peptide (BNP) level in patients with unanticoagulated NVAF. Methods: The study included 524 consecutive patients with NVAF who had undergone transesophageal echocardiography to detect intracardiac thrombus before cardioversion between January 2006 and December 2008, at Hiroshima City Asa Hospital. The exclusion criteria were as follows: paroxysmal atrial fibrillation, unknown BNP levels, prothrombin time international normalized ratio ≥2.0, and hospitalization for systemic thromboembolism. Results: Receiver operating characteristic analysis yielded optimal plasma BNP cut-off levels of 157.1 pg/mL (area under the curve, 0.91; p251.2 pg/mL was an independent predictor of LAA thrombus (odds ratio, 3.51; 95% confidence interval, 1.08–10.7; p=0.046). Conclusions: In patients with unanticoagulated NVAF, a BNP level >251.2 pg/mL may be helpful for predicting the incidence of LAA thrombus and may be used as a surrogate marker of CHF. The BNP level is clinically useful for the risk stratification of systemic thromboembolism in patients with unanticoagulated NVAF.

Rho-associated kinases play an important role in a variety of cellular functions. Although Rho-associated kinase activity has been shown to be an independent predictor for future cardiovascular events in a general population, there is no information on Rho-associated kinase activity in patients with acute coronary syndrome. We evaluated leukocyte Rho-associated kinase activity by Western blot analysis in 73 patients with acute coronary syndrome and 73 age- and gender-matched control subjects. Rho-associated kinase activity within 2 hours of acute coronary syndrome onset was higher in patients with acute coronary syndrome than in the control subjects (0.95±0.55 versus 0.69±0.31; P P =0.03 and P =0.03, respectively) and then gradually decreased to 0.83±0.52 after 7 days, 0.78±0.42 after 14 days, and 0.72±0.30 after 6 months ( P =0.22, P =0.29, and P =0.12, respectively). During a median follow-up period of 50.8 months, 31 first major cardiovascular events (death from cardiovascular causes, myocardial infarction, ischemic stroke, and coronary revascularization) occurred. After adjustment for age, sex, cardiovascular risk factors, and concomitant treatment with statins, increased Rho-associated kinase activity was associated with increasing risk of first major cardiovascular events (hazard ratio, 4.56; 95% confidence interval, 1.98–11.34; P

While hypertension has been shown to be a risk factor for vascular dementia, several studies have also demonstrated that hypertension also increases the risk of Alzheimer's disease (AD). Although the relationship between visit-to-visit blood pressure variability (VVV) and cognitive impairment, including AD, have been provided, the mechanisms remain poorly understood. This review paper focuses on the relationship of VVV with AD and summarizes the pathophysiology underlying that relationship, which appears to be mediated by arterial stiffness.

A coronary arteriovenous fistula is an abnormal connection between a coronary artery and any of four chambers in the heart. We repot a unique case with a fistulae originating from right coronary artery and draining into the right atrium via coronary sinus although Takotsubo-like left ventricular dysfunction or acute myocardial infarction was initially thought to have occurred according to the electrocardiogram finding.

We read the interesting clinical report by Jung et al,1 who investigated clinical and radiological characteristics of ischemic stroke patients with Takotsubo cardiomyopathy (TC). Jung et al1 found that ischemic lesions were mainly located in the right insular cortex (IC), which was the most frequently overlapped. However, there were little descriptions in the pathophysiology for the lesion laterality in the IC. One possible mechanism underlying TC was increased sympathetic nervous system activity.2 …

Sudden cardiac arrest is a major cause of unexpected death, as well as a major clinical issue. Primary percutaneous coronary intervention (PCI) can drastically improve outcomes among patients with ST-elevation myocardial infarction without cardiac arrest. Recent studies reported that using emergency PCI to resuscitate patients has the potential to improve their outcomes. The purpose of this review is to elucidate the effects of PCI among resuscitated patients.To the best of current understanding, no randomized clinical trial has assessed PCI for postcardiac arrest syndrome. Several observational studies suggested a positive effect of PCI for resuscitated out-of-hospital cardiac arrest (OHCA) patients, and a number of observational studies reported a limited beneficial effect. Several studies reported that a combination of therapeutic hypothermia and PCI may be feasible and effective. However, the presence of bias and unmeasured confounders in these studies may have affected the outcomes.PCI for postcardiac arrest syndrome may improve outcomes of OHCA patients; however, randomized trials of PCI for postcardiac arrest syndrome are necessary to confirm this issue. Alternative cardiopulmonary resuscitation using venoarterial extracorporeal membrane oxygenation and PCI may have the potential to improve the outcomes of refractory cardiac arrest patients.

We read the interesting recent article by Tully et al1 who found that the angiotensin receptor blocker (ARB) and β-blocker were associated with incident stroke, whereas long-term visit-to-visit blood pressure (BP) variability was not associated with that in the elderly. The mechanism underlying in the relationship between β-blocker use and increased stroke risk was suggested as compensatory hemodynamic changes associated with decreased heart rate.2 Thus, in the elderly, increased aortic stiffness and pressure wave reflection lead to increased central aortic pressures with β-blocker use.2 On the other hand, there were less explanations for the relationship between …

Background Previous study has demonstrated that metabolic syndrome (MetS) can predict cardiovascular mortality in men, but the prediction was weak for women. In the present study predictors for multiple complex coronary lesions were investigated to clarify the impact of MetS in Japanese women with acute coronary syndrome (ACS). Methods and Results Subjects were Japanese women with ACS (n=81) who underwent emergency coronary angiography and B-mode carotid ultrasonography. They were divided into 2 groups based on the number of complex plaques. Although the MetS prevalence identified using the Japanese criteria was similar between the 2 groups, using the modified ATP III criteria it was more in patients with multiple coronary lesions than in those with a single coronary lesion (p

Aims There is little knowledge about the predictors of left atrial appendage (LAA) thrombi in non-valvular atrial fibrillation (NVAF). We investigated the ability of d-dimer to predict LAA thrombi. Methods and results In this study, 925 patients with NVAF were enrolled. At the time of transoesophageal echocardiography (TEE), d-dimer levels were measured simultaneously. Significant independent predictors of LAA thrombi were the presence of congestive heart failure [odds ratio (OR) 3.10, 95% confidence interval (CI) 1.77–5.50, P < 0.0001), a history of recent embolic events (OR 3.39, 95% CI 1.90–6.04, P < 0.0001), and d-dimer levels (OR 97.6, 95% CI 17.3–595.8, P < 0.0001). Receiver operating characteristic analysis yielded an optimal cutoff value of 1.15 µg/mL for d-dimer to detect LAA thrombi. LAA thrombi were detected in 21.8% of patients with higher d-dimer values, whereas it was detected in only 3.1% of patients with lower d-dimer values. d-dimer cutoff level of 1.15 µg/mL had a negative predictive value of 97% for identifying LAA thrombi. Conclusion In patients with NVAF, d-dimer may be helpful for predicting the absence of LAA thrombi. d-dimer level was clinically useful to guide the management of patients with NVAF, especially for those complicated with congestive heart failure and/or recent embolic events.

Background The aim of the present study was to investigate the clinical implication of metabolic syndrome and carotid artery morphologies on coronary plaque vulnerability in Japanese men with acute coronary syndrome (ACS). Methods and Results Consecutive ACS Japanese men (n=225) underwent emergent coronary angiography and B-mode ultrasonography within 1 week of the acute coronary event. With a 11.3-MHz linear array transducer, the morphologies of common carotid artery were examined. Common carotid arteries with an intima-media thickness >1.1 mm and interadventitial diameter >8.0 mm were considered to be undergoing carotid artery remodeling. Patients were divided into 2 groups based on the number of complex plaques identified by coronary angiography. Abdominal obesity, low level of high-density lipoprotein and carotid artery remodeling were more often observed in patients with multiple, complex coronary plaques than in patients with a single, complex plaque (p

Recent studies have shown that visit-to-visit blood pressure (BP) variability was emerging as an independent risk factor for stroke. Although the mechanism is not fully understood, artery remodeling would be closely associated with the relationship between visit-to-visit BP variability and stroke. In addition, the class of antihypertensive agents is suggested to be an important determinant of visit-to-visit BP variability. This review article summarizes the recent literature on these topics. In the elderly hypertensives, strict BP control using calcium channel blockade would play a crucial role to prevent stroke via reducing the visit-to-visit BP variability.

Although the AAI pacing mode has been shown to be electromechanically superior to the DDD pacing mode in sick sinus syndrome (SSS), there is evidence suggesting that during AAI pacing the presence of natural ventricular activation pattern is not enough for hemodynamic benefit to occur. Myocardial performance index (MPI) is a simply measurable Doppler-derived index of combined systolic and diastolic myocardial performance. The aim of this study was to investigate whether AAI pacing mode is electromechanically superior to the DDD mode in patients with SSS by using Doppler-derived MPI.Thirty-nine SSS patients with dual-chamber pacing devices were evaluated by using Doppler echocardiography in AAI mode and DDD mode. The optimal atrioventricular (AV) interval in DDD mode was determined and atrial stimulus-R interval was measured in AAI mode. The ratio of the atrial stimulus-R interval to the optimal AV interval was defined as relative AV interval (rAVI) and the ratio of MPI in AAI mode to that in DDD mode was defined as relative MPI (rMPI).The rMPI was significantly correlated with atrial stimulus-R interval and rAVI (r = 0.57, P = 0.0002, and r = 0.67, P0.0001, respectively). A cutoff point of 1.73 for rAVI provided optimum sensitivity and specificity for rMPI1 based on the receiver operator curves.Even though the intrinsic AV conduction is moderately prolonged, some SSS patients with dual-chamber pacing devices benefit from the ventricular pacing with optimal AV interval. MPI is useful to determine the optimal pacing mode in acute experiment.

ObjectivesThe purpose of this study was to determine the relationship between matrix metalloproteinases (MMPs)-1, -2, and -9, and tissue inhibitors of metalloproteinases (TIMP)-1 and the atrial structural remodeling during atrial fibrillation (AF).BackgroundMatrix metalloproteinases, a family of proteolytic enzymes and TIMPs, regulate the extracellular matrix turnover in cardiac tissue.MethodsTissue samples were obtained from 25 patients without a history of AF (regular sinus rhythm [RSR]) and 13 patients with AF (paroxysmal AF: 6, chronic AF 7) undergoing cardiac operations. We performed a western blotting analysis of the MMP-1, -2, and -9, and quantitatively analyzed the expression of the MMP-9 and TIMP-1 by real time polymerase chain reaction and ELISA. The localization of the MMP-9 was investigated by in situ zymography and immunohistochemistry.ResultsThe active form of the MMP-9 was significantly increased in the AF group in comparison to that in the RSR group (p < 0.05), but there were no differences between the groups in the protein level of the latent form of the MMP-9 and active and latent forms of the MMP-1 and MMP-2. We also demonstrated that the expression of the MMP-9 was significantly more increased in the atria of the AF group than in that of the RSR group for both the messenger ribonucleic acid (mRNA) (AF: RSR; 1: 1.5) and protein levels (AF: RSR; 3.9 ± 1.3 : 1.5 ± 0.4 ng/mg atrium). The expression level of the MMP-9 was also higher in the PAF group than in the RSR group, however, the diameter of the left atrium was similar in both groups. The gelatinase activity and left atrium diameter were positively correlated (p < 0.05, R = 0.766). The relative expression of the mRNA for the monocyte chemoattractant protein-1 was higher in the AF group than in the RSR group. Immunohistochemical analysis revealed that the MMP-9 was distributed within the perivascular area and under the epicardium of the atria.ConclusionsWe clearly showed that the expression of the MMP-9 increased in fibrillating atrial tissue, which may have contributed to the atrial structural remodeling and atrial dilatation during AF.

Objectives We investigated the relationship between ultrasonographic features of the carotid artery and the angiographic features of coronary plaques in acute coronary syndrome (ACS). Background The carotid intima-media thickness (IMT) may be a marker of advanced coronary artery disease. Methods Consecutive ACS patients (N = 125) underwent B-mode ultrasonography within one week of the acute coronary event. Using a 7.5-MHz linear array transducer, the common carotid IMT, interadventitial diameter, and luminal diameter were examined. Carotid plaques were also assessed. Then patients were divided into two groups based on the number of complex plaques identified by coronary angiography. Results The carotid IMT of 75 patients with multiple complex coronary plaques was significantly larger than that of 50 patients with solitary plaques (p Conclusions In ACS, multiple complex coronary plaques are associated with positive carotid remodeling, suggesting that plaque vulnerability may be a systemic phenomenon.

The slow flow (SF) phenomenon is more prevalent in patients with acute coronary syndrome (ACS), who frequently exhibit vulnerable plaques in remote coronary arteries. We aimed to clarify the impact of nonculprit plaque characteristics on the occurrence of SF using multidetector computed tomography (MDCT).The study population comprised 180 consecutive patients with non-ST-segment elevation ACS (NSTE-ACS) who underwent MDCT before intervention. The characteristics of culprit and nonculprit lesions were compared between patients with and without SF.SF was observed in 43 (23.8%) of the 180 patients. The prevalence of positive remodeling (PR), low-attenuation plaque (LAP), and napkin-ring sign (NRS) in culprit lesion was significantly higher in the SF group than in the non-SF group (86.1% vs. 39.4%; p0.001, 81.4% vs. 18.3%; p0.001, and 65.1% vs. 16.1%; p0.001, respectively). The same result was observed for nonculprit lesions (58.1% vs. 14.6%; p0.001, 45.2% vs. 6.6%; p0.001, and 14.3% vs. 4.9%; p0.04, respectively). Multivariate analysis revealed LAP [odds ratio (OR), 12.8; 95% confidence interval (CI), 3.7-54.7; p0.001], and NRS (OR, 5.1; 95% CI, 1.3-25.3; p=0.03) in culprit lesions and PR (OR, 4.7; 95% CI, 1.1-22.2; p=0.04) in nonculprit lesions were independently associated with SF.The plaque characteristics of nonculprit lesions are associated with the occurrence of SF during percutaneous coronary intervention. Assessment of plaque characteristics of both culprit and nonculprit lesions using MDCT may be useful for the prediction of SF.