Shuichi Katsushika

Alterations in cardiac function and subcellular membrane activities after hypervitaminosis D3

The present study was designed to induce massive accumulation of calcium in the myocardium and to evaluate the effect of calcium overload on myocardial contractile function and biochemical activity of cardiac subcellular membranes. Rats were treated with an oral administration of 500,000 units/kg of vitamin D3 for 3 consecutive days, and their hearts were sampled on the 5th day for biochemical analysis. On the 4th and 5th days, heart rate, mean aortic pressure, left ventricular systolic pressure and left ventricular dP/dt were significantly lowered in vitamin D3-treated rats, demonstrating the existence of appreciable myocardial contractile dysfunction. Marked increases in the myocardial calcium (67-fold increase) and mitochondrial calcium contents (24-fold increase) were observed by hypervitaminosis D3. Mitochondrial oxidative phosphorylation and ATPase activity were significantly reduced by this treatment. A decline in sarcolemmal Na+, K+-ATPase activity was also observed, while relatively minor or insignificant changes in calcium uptake and ATPase activities of sarcoplasmic reticulum were detectable. Electron microscopic examination revealed calcium deposits in the mitochondria after vitamin D3 treatment. The results suggest that hypervitaminosis D3 produces massive accumulation of calcium in the myocardium, particularly in the cardiac mitochondrial membrane, which may induce an impairment in the mitochondrial function and eventually may lead to a failure in the cardiac contractile function.

Coronary remodeling of proximal and distal stenotic atherosclerotic plaques within the same artery by intravascular ultrasound study

The aim of this intravascular ultrasound study was to compare the type and the degree of vessel remodeling in proximal and distal de novo lesions within the same coronary artery in patients with stable angina pectoris. Seventy-six de novo coronary artery lesions in 38 coronary arteries of 38 patients were imaged by intravascular ultrasound. The vessel area (VA) within the external elastic lamina and the lumen area (LA) were measured, and the wall area (VA-LA) was calculated at the lesion site, and the proximal and distal reference sites. The VA ratio was defined as (lesion VA/average of the proximal and distal reference VAs) to represent the degree of vessel remodeling. The proximal coronary segments showed compensatory enlargement more often (68% vs 29%, p < 0.01) than the distal segments, and the VA ratio at the lesion site was significantly larger (1.1 +/- 0.3 vs 1.0 +/- 0.2, p <0 .01) in proximal segments than in distal segments. The type of coronary remodeling was discordant in 61% and concordant in only 39% of coronary arteries between the proximal and distal segments. The type of coronary remodeling of proximal and distal coronary lesions was inhomogeneous, even within the same vessel. Proximal coronary segments showed more prominent compensatory enlargement than distal segments, which have a similar degree of luminal narrowings.

Hypertrophic obstructive cardiomyopathy due to a novel T-to-A transition at codon 624 in the β-myosin heavy chain (β-MHC) gene possibly related to the sudden death

Many missense mutations in the beta-myosin heavy chain have been reported in patients with hypertrophic obstructive cardiomyopathy (HOCM). However, the controversy is present whether the mutation accompanying the change of electric charge is related with poorer prognosis. The proband, a 48-year-old female, of the family was diagnosed clinically as HOCM, and a structural analysis of the cardiac beta-MHC gene showed that the proband and her junior daughter had a novel mutation with T to A transition in codon 624 replacing tyrosine with asparagine, which was not present in her husband, elder daughter and son. The probands husband, son and two daughters were healthy except that the ECG of junior daughter (15-year-old) showed complete right bundle branch block. Probands mother died suddenly after the delivery of the proband and the proband also collapsed suddenly. The occurrence of sudden death in proband and her mother suggested that HOCM with this novel mutation might be associated with a high risk of sudden death irrespective of the absence of charge alteration.

Primary Mural Endocarditis Without Valvular Involvement

Primary mural endocarditis is an extremely rare infection in which nonvalvular endocardial involvement is seen without any cardiac structural abnormalities such as ventricular septal defects. The rapid and precise diagnosis of this disease remains challenging. We present 2 cases (67‐ and 47‐year‐old male patients) of pathologically confirmed primary mural endocarditis that could have been detected by initial transthoracic echocardiography in the emergency department. Transthoracic echocardiography and transesophageal echocardiography play critical roles in the early recognition and confirmation of primary mural endocarditis.

Successful diagnosis of an atypical prosthetic vascular graft infection without perivascular abscess: luminal vegetation as the hidden septic source.

A 62-year-old woman with a vascular prosthesis for a common hepatic artery aneurysm (3 years ago) was hospitalized because of a 2-week history of lumbago and fever. Six months previously, she was hospitalized at another medical facility for 1 month because of a fever of unknown pathogenesis. Laboratory examination revealed moderate inflammation with an elevated C-reactive protein level of 6.5 mg/dL and a white blood cell count of 7070/mm3. Initial 8-row multi-detector computed tomography (CT) with contrast agent in the emergency department did not show any focus for the origin of the fever. She was referred to the orthopedic surgery department, and MRI of the pelvis revealed inflammation of the left sacroiliac joint (Figure 1). Her first 2 sets of blood cultures were positive for Streptococcus anginosus . Intravenous administration of ampicillin/cloxacillin sodium was started. She was then transferred to the cardiology department for the evaluation of septicemia, which could have been caused by infectious endocarditis. A transthoracic echocardiogram showed severe aortic regurgitation, which was not seen at the time of previous surgery for the vascular prosthesis (Figure 2A). However, a transesophageal echocardiogram only detected a small degenerative change in the right coronary cusp of the aortic valve, which could be healed …

Cardiac Asystole Triggered by Temporal Lobe Epilepsy with Amygdala Enlargement

A 25-year-old previously healthy man was hospitalized for syncope. While standing, he suddenly lost consciousness, followed by a generalized tonic clonic seizure. An electrocardiogram demonstrated asystole. No cardiac abnormalities were detected on the echocardiogram, cardiac magnetic resonance imaging (MRI), positron emission tomography, or a coronary angiogram. An electrophysiological study showed normal sinus node and atrioventricular node function. An electroencephalogram revealed small spike waves in the fronto-temporal region. Brain MRI demonstrated a left-sided amygdala enlargement. To the best of our knowledge, this is the first case of temporal lobe epilepsy with an amygdala enlargement that induced cardiac asystole.

Rapid Swelling of Infarcted Myocardium Soon after Primary Percutaneous Coronary Intervention: A Sign of Critical Reperfusion Hemorrhage

A 64-year-old man with a history of diabetes mellitus presented with acute myocardial infarction. He received successful primary percutaneous coronary intervention (PPCI) of the circumflex coronary artery, with good reflow at 8 hours after the onset of chest pain (Fig. 1A–C, movie clip S1). Intravascular ultrasound images at the site of occlusion denied the existence of coronary dissection. He had received oral prasugrel and aspirin along with intravenous heparin prior to the PPCI. Six hours after the PPCI, echocardiography revealed a massively thickened, infarcted myocardium from the lateral to the posterior wall, with granular echoes (Fig. 2B), as compared to the images before PPCI (Fig. 2A). On day 2, he developed cardiac tamponade (Fig. 3) and was treated with open pericardiocentesis. We postulated that the cause of cardiac tamponade might be bleeding from the infarcted myocardium, because the pericardial effusion was bloody. Cardiac magnetic resonance imaging (CMR) was performed on day 6, and T2* imaging clearly confirmed the presence of a massive intramyocardial hemorrhage (IMH) with transmural hypointensity in the infarcted myocardium (Fig. 4, arrowheads). Thereafter, the patient’s course was uneventful. Rapid swelling of infarcted myocardium after PPCI is a rare phenomenon on echocardiography. The mechanism might be a massive transmural IMH as