Late onset of coronary ostial stenosis following surgical aortic valve replacement in a patient with anomalous origin of the right coronary artery.

Surgical aortic valve replacement (SAVR) in patients with anomalous origination of a coronary artery from the opposite sinus is associated with risk for myocardial ischemia during the perioperative period. [1] However, iatrogenic coronary ostial stenosis (ICOS) generally occurs within the first 6 months after SAVR. We present an unusual case of a 74-year-old man with anomalous origination of the right coronary artery from the left coronary sinus, who developed effort angina due to ICOS 19 months following SAVR and ascending aorta replacement.

Platypnea-Orthodeoxia Syndrome Associated with Spontaneously Ruptured Chordae Tendineae of Tricuspid Valve.

• POS is a rare clinical condition. • Symptoms are upright posture dyspnea and arterial desaturation. • Supine and sitting position oxygen saturation levels suggest right-to-left shunt.

Ablation of cardiac TIGAR preserves myocardial energetics and cardiac function in the pressure overload heart failure model.

Despite the advances in medical therapy, the morbidity and mortality of heart failure (HF) remain unacceptably high. HF results from reduced metabolism-contraction coupling efficiency, so the modulation of cardiac metabolism may be an effective strategy for therapeutic interventions. Tumor suppressor p53 (TP53) and its downstream target TP53-induced glycolysis and apoptosis regulator (TIGAR) are known to modulate cardiac metabolism and cell fate.

First-in-Man Clinical Pilot Study Showing the Safety and Efficacy of Intramuscular Injection of Basic Fibroblast Growth Factor With Atelocollagen Solution for Critical Limb Ischemia.

Background: Therapeutic angiogenesis with basic fibroblast growth factor (bFGF) with atelocollagen was confirmed in a study using a limb ischemia mouse model. Because the number of elderly patients with critical limb ischemia (CLI) is increasing, particularly that caused by arteriosclerosis obliterans (ASO), the development of less invasive angiogenesis therapies desired.

Methods and results: This first-in-man clinical study was designed to assess the safety and efficacy of i.

Cardiac-Specific Bdh1 Overexpression Ameliorates Oxidative Stress and Cardiac Remodeling in Pressure Overload-Induced Heart Failure.

Background: Energy starvation and the shift of energy substrate from fatty acids to glucose is the hallmark of metabolic remodeling during heart failure progression. However, ketone body metabolism in the failing heart has not been fully investigated.

Methods And Results: Microarray data analysis and mitochondrial isobaric tags for relative and absolute quantification proteomics revealed that the expression of D-β-hydroxybutyrate dehydrogenase I (Bdh1), an enzyme that catalyzes the NAD/NADH coupled interconversion of acetoacetate and β-hydroxybutyrate, was increased 2.

-Glutamate is metabolized in the heart mitochondria.

-Amino acids are enantiomers of L-amino acids and have recently been recognized as biomarkers and bioactive substances in mammals, including humans. In the present study, we investigated functions of the novel mammalian mitochondrial protein 9030617O03Rik and showed decreased expression under conditions of heart failure. Genomic sequence analyses showed partial homology with a bacterial aspartate/glutamate/hydantoin racemase.

Activation of PPAR-α in the early stage of heart failure maintained myocardial function and energetics in pressure-overload heart failure.

Failing heart loses its metabolic flexibility, relying increasingly on glucose as its preferential substrate and decreasing fatty acid oxidation (FAO). Peroxisome proliferator-activated receptor α (PPAR-α) is a key regulator of this substrate shift. However, its role during heart failure is complex and remains unclear.

Usefulness of peripheral arterial signs in the evaluation of aortic regurgitation.

Background: Early diagnosis and optimal timing of surgical repair for chronic aortic regurgitation (AR) are topics of interest, because left ventricular compensation delays the clinical signs of the early stages of left ventricular dysfunction. Various physical signs have been described as indicators of chronic AR, but AR screening can be difficult depending on the proficiency of primary care providers. The recent use of the cardio-ankle vascular index (CAVI) measurement to assess peripheral atherosclerosis may detect AR objectively and simply because its arterial pulse wave configuration is closely related to the physical signs of AR.

Pyk2 aggravates hypoxia-induced pulmonary hypertension by activating HIF-1α.

Pulmonary arterial hypertension (PAH) is a refractory disease characterized by uncontrolled vascular remodeling and elevated pulmonary arterial pressure. Although synthetic inhibitors of some tyrosine kinases have been used to treat PAH, their therapeutic efficacies and safeties remain controversial. Thus, the establishment of novel therapeutic targets based on the molecular pathogenesis underlying PAH is a clinically urgent issue.

Oxidative post-translational modifications develop LONP1 dysfunction in pressure overload heart failure.

Background: Mitochondrial compromise is a fundamental contributor to heart failure. Recent studies have revealed that several surveillance systems maintain mitochondrial integrity. The present study evaluated the role of mitochondrial AAA+ protease in a mouse model of pressure overload heart failure.

Inhibition of p53 preserves Parkin-mediated mitophagy and pancreatic β-cell function in diabetes.

Mitochondrial compromise is a fundamental contributor to pancreatic β-cell failure in diabetes. Previous studies have demonstrated a broader role for tumor suppressor p53 that extends to the modulation of mitochondrial homeostasis. However, the role of islet p53 in glucose homeostasis has not yet been evaluated.

Masquerading bundle branch block as a marker of poor prognosis.

Masquerading bundle branch block is a rare and unique finding on a 12-lead electrocardiogram, consisting of the pattern of right bundle branch block in the precordial leads and left bundle branch block in the limb leads. We experienced a 77-year-old woman with masquerading bundle branch block. She had been well, but died suddenly 9 months after the diagnosis of masquerading bundle branch block.

Intramyocardial calcification in a patient with apical hypertrophic cardiomyopathy.

Intramyocardial calcification is a very rare condition. We report a case of a 72-year-old man with apical hypertrophic cardiomyopathy, who was initially suspected of having a thrombus in the left ventricular apex on echocardiography, but was finally diagnosed as having apical intramyocardial calcification on multidetector computed tomography. The mechanism of developing intramyocardial calcification remains to be elucidated, but the patient has been stable for more than 2 years.

Myocardial perfusion abnormality in the area of ventricular septum-free wall junction and cardiovascular events in nonobstructive hypertrophic cardiomyopathy.

Myocardial perfusion abnormality in the left ventricle is known to be prognostic in patients with hypertrophic cardiomyopathy (HCM). Magnetic resonance imaging and necropsy studies on HCM hearts revealed myocardial lesions predominating in the area of ventricular septum-free wall junction. We assessed perfusion abnormality in this area and correlated it with the prognosis of HCM patients.

Three-layer ultrasonic tissue characterization of the ventricular septum is predictive of prognosis in patients with non-obstructive hypertrophic cardiomyopathy.

Aims: A necropsy study of patients with hypertrophic cardiomyopathy (HCM) who died at a young age exhibited marked disarray and fibrosis in the mid-wall layer of the left ventricular (LV) myocardium. We assessed ultrasonic tissue characteristics in the three layers of the ventricular septum (VS), and correlated the result with long-term prognosis in HCM.

Methods And Results: The magnitude of cyclic variation of integrated backscatter (CV-IB) was calculated in the three layers of the VS and the whole aspect of the LV posterior wall in 58 non-obstructive HCM patients and 20 healthy controls.

Chronotropic incompetence and autonomic dysfunction in patients without structural heart disease.

Aims: An attenuated heart rate response to exercise, termed chronotropic incompetence (CI), has been reported to be an independent predictor of cardiovascular mortality. We examined the change in autonomic function during exercise testing and correlated the results with CI.

Methods And Results: Exercise testing using a bicycle ergometer was performed in 172 patients who had no evidence of cardiac disease.