There are conflicting reports regarding the occurrence of cardiovascular events after a major earthquake. To understand the impact of the Great East Japan Earthquake on cardiovascular events, we retrospectively examined the clinical records prepared by emergency room physicians between 2009 and 2011 (n = 66,244), and compared the occurrence of these events between 2011 and 2009, and 2011 and 2010. There was a significant increase in the number of patients with cardiovascular events during the 3 week period after the earthquake in 2011 (n = 106) compared with that during the same period in 2009 (n = 72) or 2010 (n = 65) (P = 0.002). The number of patients with acute coronary syndrome or congestive heart failure in March 2011 was significantly increased compared with 2009 or 2010, however, there were no significant increases in 2011 in other cardiovascular events including stroke, aortic dissection, pulmonary thromboembolism, or out-of-hospital cardiac arrest compared with 2009 or 2010. These findings suggest that the incidence of cardiovascular events may have been heterogeneous after the disaster.
Residual risk of cardiovascular disease might stem, at least partially, from low serum concentrations of n-3 polyunsaturated fatty acid (PUFA). The purpose of this study was to evaluate the effects of ezetimibe on serum lipids and PU-FAs in patients with coronary artery disease who were intolerant of new or high-dose statin therapy. The study population consisted of 13 patients who were intolerant of new statin therapy and 10 patients who were intolerant of high-dose statin therapy for the treatment of low-density lipoprotein (LDL) cholesterol. Patients who were intolerant of high-dose statin therapy continued taking a statin, but at a lower dose during the study period. Blood samples were collected before and 12 weeks after ezetimibe (10 mg). We measured serum lipids and PUFAs including dihomo-γ-linolenic acid, arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid. Ezetimibe significantly decreased LDL cholesterol (138 ± 19 mg/dL to 97 ± 34 mg/dL, P < 0.01), but did not significantly affect high-density lipoprotein cholesterol, triglyceride, or any of the PUFAs measured during the follow-up period. Consequently, it did not affect the ratio of EPA to AA (0.40 ± 0.17 to 0.43 ± 0.18, P = ns) or the ratio of n-3 PUFA to n-6 PUFA (1.10 ± 0.39 to 1.09 ± 0.36, P = ns) during the follow-up period. Ezetimibe in combination with a low-dose statin, or as monotherapy in statin-intolerant patients, decreased LDL cholesterol, but did not significantly affect serum PUFA concentrations in patients with coronary artery disease.
This study sought to examine the prevalence of insomnia and its association with depression, anxiety, and medical comorbidities in patients after an acute coronary syndrome (ACS). Insomnia increases risk of recurrent cardiac events in ACS patients, but little is known about the prevalence and clinical correlates of insomnia in this setting. Patients (n = 102, 58.3 ± 10.6 years-old) admitted for ACS to a cardiology service at an urban academic medical center completed the Insomnia Severity Index, Epworth Sleepiness Scale, and measures of depression and anxiety. A subset (n = 20) completed ambulatory polysomnography (PSG) in their homes several weeks after discharge. Moderate or severe insomnia was reported by 37% of patients during hospitalization and was associated with 76 minutes more wake after sleep onset measured by home PSG. Although depression and insomnia were strongly associated, about 1 in 4 patients with insomnia did not report significant depressive symptoms. Sleep apnea was documented in 80% of patients on PSG, but insomnia was not associated with sleep apnea, periodic limb movements, demographic factors, or medical conditions other than liver disease. Insomnia is present in over one-third of ACS patients during hospitalization, but at-risk patients could not be readily identified by demographic or medical factors or by depression symptoms.
Noninvasive detection of coronary artery stenosis usually requires a stress test in patients without left ventricular (LV) regional wall motion abnormalities (RWMA). In contrast, abnormal regional LV relaxation caused by ischemia may persist beyond recovery from transient ischemia. The aim of the present study was to determine whether segmental analysis of abnormal regional LV relaxation using the strain imaging diastolic index (SI-DI) at rest could predict coronary artery stenosis in the three major vessels in patients without LV dysfunction or RWMA. We performed 2D speckle tracking echocardiography and coronary angiography in 85 patients without RWMA with suspected coronary artery disease. Patients with LV dysfunction or acute coronary syndrome were excluded. Echocardiographic images of the LV were obtained in the apical 2-, 3-, and 4-chamber views and divided into 6 segments. In each segment, SI-DI derived from transverse strain imaging was determined. Forty-eight patients had significant coronary artery stenosis (≥ 70%). The optimal cutoff values of SI-DI were 60.5% in the mid anteroseptal segment for detecting left anterior descending artery stenosis (sensitivity, 83.3%; specificity, 81.1%), 60.5% in the basal anterolateral segment for detecting left circumflex artery stenosis (sensitivity, 80.9%; specificity, 90.3%), and 61.5% in the basal inferior segment for detecting right coronary artery stenosis (sensitivity, 74.1%; specificity, 77.8%). A segmental analysis of SI-DI at rest predicted coronary artery stenosis in the three major vessels in patients without RWMA. This noninvasive method may be useful for detecting coronary artery stenosis without a stress test.
Metabolic syndrome (MS) is currently considered to be a risk factor for arteriosclerotic disease. The accumulation of visceral fat leads to arteriosclerotic disease after other risk factors have developed and either direct or mutual effects occur. The aim of this study was to verify whether visceral fat serves as an independent coronary risk factor. A total of 3157 patients who had undergone multi-detector computed tomography (MDCT) were analyzed via computed tomographic angiography and the measurement of their visceral fat area. Coronary arteries with > 70% stenosis were considered to be significant. The visceral fat area was measured at the umbilical level, and an area of 100 cm2 or more was defined as visceral obesity. Coronary risk factors (ie, hypertension, dyslipidemia, diabetes mellitus, family history, and smoking) were obtained from the patient medical records. The patients were divided into two groups: a visceral obesity group, 1130 patients (137.0 ± 31.1 cm2) and a nonvisceral obesity group, 2027 patients (57.3 ± 25.8 cm2). A significant difference in the incidence of coronary stenosis between the two groups was observed. According to multivariable analysis, the factors affecting coronary stenosis were age, gender, dyslipidemia, diabetes mellitus, and the ratio of visceral to subcutaneous fat. Visceral obesity was not found to be an independent coronary risk factor. Visceral obesity demonstrated the predominant presence of coronary risk factors.
Persistent atrial fibrillation (AF) is characterized by electrical remodeling, ie, marked decreases in the atrial effective refractory period (ERP), ERP rate adaptation, and atrial conduction velocity. Little information is available on the effects of class III antiarrhythmic drugs on the remodeled atrium. We studied the effects of the class III antiarrhythmic drugs nifekalant, ibutilide, and amiodarone on rate-dependent changes in atrial action potential duration in patients with persistent AF. Right atrial (RA) monophasic action potential duration (MAPD) and intra-atrial conduction time (IACT) were measured at pacing cycle lengths (CLs) of 800, 700, 600, 500, 400, 350, 300, and 250 ms before and after administration of nifekalant (0.4 mg/kg + 0.3 mg/kg/hr, iv), amiodarone (5 mg/kg, iv), or ibutilide (0.01 mg/kg, iv) in 31 patients after successful internal cardioversion of chronic AF of > 2 months duration. Nifekalant and ibutilide significantly increased RA MAPD and the ERP at each CL in a reverse rate-dependent manner. Amiodarone did not affect RA MAPD. Nifekalant did not affect IACT, whereas amiodarone increased IACT at each CL in a rate-dependent manner, and ibutilide increased IACT at CLs ≤ 350 ms. The atrial electrophysiologic effects of the class III antiarrhythmic drugs nifekalant, amiodarone, and ibutilide differ, depending on the degree of electrical and structural remodeling and the effects of the drugs on the depolarizing and repolarizing currents.
Non-contact array mapping studies have demonstrated the existence of a line of conduction block along the septopulmonary bundle area and the posterior left atrial (LA) roof during sinus rhythm (SR). However, little is known of the global LA activation pattern during SR using a high-density contact bipolar mapping system. High-density contact bipolar isochronal mapping (bipolar mapping sites: 292 [IQR 250-348] points) of the LA was performed during SR with the NavX mapping system in 20 patients with paroxysmal atrial fibrillation (AF) and 11 patients with non-paroxysmal AF. The earliest endocardial breakthrough in the the LA from the right atrium (RA) during SR occurred in the anterosuperior LA (77%) or anterior to the right pulmonary veins (23%), and the breakthrough site did not differ between patients with paroxysmal and non-paroxysmal AF. Regardless of the site of breakthrough, the LA activation pattern was homogeneous, and no line of functional block was observed in any patient. Total LA activation time was significantly longer in non-paroxysmal AF patients than in paroxysmal AF patients (95.1 ± 4.3 ms versus 78.3 ± 3.2 ms, P = 0.0040). Contactbased bipolar LA endocardial activation mapping revealed a homogeneous LA activation pattern during SR, regardless of the between-group difference in activation time and the between-patient difference in sites of earliest LA endocardial breakthrough from the RA.
A 73-year old man received an implantable loop recorder (ILR) for the evaluation of transient loss of consciousness (TLOC) spells. His medical history was without any epileptic convulsions or automatism. ILR recording during a spontaneous episode revealed the presence of a regular, narrow QRS complex tachycardia associated with low-amplitude, high-frequency, continuous or discontinuous artifacts, consistent with myopotentials. During the event, the regular, lowamplitude continuous signals gradually became discontinuous, with a prolongation of the inter-signal cycle length, until their disappearance after manual activation of the ILR. The patient was diagnosed as experiencing subclinical tonic-clonic epileptic seizures. Antiepileptic drug treatment was initiated, and the patient has remained free of TLOC symptoms during 13 months follow-up.
Systolic anterior motion (SAM) of the mitral valve after aortic valve replacement (AVR) for severe aortic stenosis (AS) is one of the causes of perioperative left ventricular outflow tract (LVOT) obstruction in older patients. A 90-yearold woman underwent AVR with a 19-mm bioprosthesis for symptomatic aortic valve stenosis. Preoperative transthoracic echocardiography (TTE) showed left ventricular hypertrophy, with LVOT obstruction and mild mitral regurgitation (MR). Intraoperative transesophageal echocardiography and postoperative TTE showed that the degree of MR was unchanged after surgery. The patient’s postoperative course was uneventful. However, she developed shortness of breath 6 months after discharge. A subsequent TTE showed significant LVOT obstruction and SAM, which resulted in moderate to severe MR. Because of the patient’s advanced age, cibenzoline was administered to decrease the left ventricular pressure gradient (LVPG) and improve the left ventricular diastolic function. Two months after administration of cibenzoline, a TTE showed decreased LVPG, trivial MR, and the absence of SAM. This case clearly demonstrated that cibenzoline improved the SAM of the mitral valve that arose after AVR for AS in a remote postoperative period.
Prevalent atrial fibrillation (AF) in patients with hypertrophic cardiomyopathy (HCM) represents an important issue with regard to stroke events caused by embolization and is associated with high mortality. Increased epicardial adipose tissue (EAT), which shows high metabolic activity, can locally influence the activity of the autonomic ganglia, enhancing autonomic dysregulation and increasing the likelihood of AF. We tested the hypothesis that EAT is associated with prevalent AF in HCM patients. Sixty-two patients with idiopathic HCM diagnosed on the basis of ultrasound cardiography findings and histopathological evaluation of myocardium obtained by right ventricular biopsy underwent cardiac magnetic resonance imaging to estimate the extent of EAT. EAT area was significantly higher in the group with AF episodes than in the group without. An increased incidence of AF was found to be significantly related to an increase in EAT, and this association persisted after adjustment for body mass index, sex, and age. Time domain measures of heart rate variability measured by Holter electrocardiography, standard deviation of normal to normal, and standard deviation of the average of normal to normal were negatively related to EAT area. EAT was positively correlated with intraventricular septal thickness and cystatin C level and negatively correlated with the 24-hour creatinine clearance rate. Increased EAT area in HCM patients is significantly related to the presence of AF, which is associated with changes in baseline autonomic nervous tone, left ventricular mass, and chronic kidney disease.
The clinical course and medical treatment of patients with congestive heart failure (CHF) complicating acute myocardial infarction (AMI) are not well established, especially in patients with concomitant renal dysfunction. We performed a retrospective analysis of the prospective Korean Acute Myocardial Infarction Registry to assess the medical treatments and clinical outcomes of patients with CHF (Killip classes II or III) complicated by AMI, in the presence or absence of renal dysfunction. Of 13,498 patients with AMI, 2769 (20.5%) had CHF on admission. Compared to CHF patients with preserved renal function, in-hospital mortality and major adverse cardiac events were increased both at 1 month and at 1 year after discharge in patients with renal dysfunction (1154; 41.7%). Postdischarge use of aspirin, betablockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, or angiotensin II receptor blockers and statins significantly reduced the 1-year mortality rate for CHF patients with renal dysfunction; such reduction was not observed for those without renal dysfunction, except in the case of aspirin. Patients with CHF complicating AMI, which is accompanied by renal dysfunction, are at higher risk for adverse cardiovascular outcomes than patients without renal dysfunction. However, they receive fewer medications proven to reduce mortality rates.
Impaired renal function is a strong predictor of mortality in chronic heart failure (CHF). However, the impact of chronic kidney disease (CKD) on prognostic factors has not been rigorously examined in CHF. The purpose of this study was to compare prognostic factors between CHF patients with and without CKD. Consecutive 505 patients with CHF, who performed cardiopulmonary exercise testing before discharge, were enrolled. Patients were divided into two groups: CKD group (eGFR < 60 mL/minute/1.73m2, n = 213) and non-CKD group (eGFR ≥ 60 mL/minute/1.73m2, n = 292). The patients were followed up to register cardiac events including cardiac death and re-hospitalization due to worsening heart failure. There were 115 events during the follow-up period (746 ± 238 days), and the cardiac event rate was higher in the CKD group than in the non-CKD group (34% versus 14%, P < 0.001). Multivariate Cox hazard analysis demonstrated that body mass index (P < 0.001), log BNP (P < 0.001), peak VO2 (P < 0.05), and left atrial dimension (P < 0.05) were independent parameters to predict cardiac events after discharge in the non-CKD group. In contrast, peak VO2 (P < 0.01), log BNP (P < 0.01), and the concentrations of hemoglobin (P < 0.05) and uric acid (P < 0.05) were independent prognostic factors in the CKD group. Prognostic factors were different between CHF patients with and without CKD, and this should be considered when managing CHF patients with CKD.
A formula derived by using large elastic deformation for the contraction of the myocardium is used to describe the pressure-volume relation (PVR) in the heart left ventricle, it is also used to calculate a mathematical expression for the non-linear end-systolic pressure-volume relation (ESPVR) in the left ventricle. An important feature of the mathematical formalism used is the inclusion of the isovolumic pressure Piso (equal active pressure generated by the myocardium) in the formalism describing the PVR. Relations between the ejection fraction (EF) and parameters describing the non-linear ESPVR are presented. It is shown that the non-linear ESPVR offers a rich collection of parameters that can be used to study the performance of the ventricles, like the areas under the ESPVR (units of energy) or the ordinates of the ESPVR (units of pressure), slopes and intercepts of the curves involved. The mathematical procedure can be easily implemented in a non-invasive way in routine clinical work when ratios of variables are calculated, it necessitates only the non-invasive measurement of the dimensions of the ventricles. Applications to clinical data published in the literature are presented, and they give results that show the consistency of the mathematical formalism used. The implications of the results of this research work on the study of the problem of heart failure with normal or preserved ejection fraction (HFpEF) are discussed.
Heart transplantation (HTx) is an established therapy for stage D heart failure due to recent advances in immunosuppressive regimens. However, antibody-mediated rejection remains an unsolved problem because of its refractoriness to standard immunosuppressive therapy with high mortality and graft loss. We experienced a 16-year old patient with hemodynamic compromise caused by both cellular and antibody-mediated rejection 12 years after HTx. The rejection was refractory to repeated steroid pulse treatment, intravenous immunoglobulin administration, and intensifying immunosuppression including addition of everolimus. Eventually, she was successfully treated with repeated plasma exchange accompanied by a single administration of the anti-CD20 monoclonal antibody rituximab.
We report the case of a 69-year-old male whose left circumflex coronary artery was perforated immediately after implantation of an Endeavor zotarolimus-eluting stent (E-ZES). Despite successful hemostasis by long balloon inflation, a coronary pseudoaneurysm remained at the E-ZES-implanted segment. Coronary angiography performed one year after the coronary perforation showed the pseudoaneurysm had disappeared. Simultaneous optical coherence tomography and coronary angioscopy revealed that stent struts of the E-ZES were fully covered with thick neointima. This is the first case report of a relatively rapid healing process for an E-ZES-related coronary pseudoaneurysm.