Basal cardiomyopathy develops in rabbits with ventricular tachyarrhythmias induced by a single injection of adrenaline.

We have recently demonstrated that basal cardiomyopathy develops in rabbits with ventricular tachyarrhythmias that have been induced by electrical stimulation of the cervical vagus. This study investigated whether similar basal cardiomyopathy would develop in rabbits with ventricular tachyarrhythmias induced by a single injection of adrenaline. Adrenaline was intravenously infused for 10-360 seconds in anesthetized rabbits. Colloidal carbon was injected after adrenaline infusion. Wall movement velocity of the left ventricular base was assessed by tissue Doppler echocardiography. Animals were killed either 1 week or 3-4 weeks later. Pathological lesions were identified by deposits of carbon particles. Animals were divided into two groups according to the infused dose of adrenaline. The small-dose group (group S, n = 15) received 1-10 µg and the large-dose group (group L, n = 23) received 15-60 µg of adrenaline. Adrenaline infusion induced premature ventricular contractions followed by monomorphic ventricular tachycardias in 22 of 23 animals in group L, but in only 1 of 15 animals in group S. Wall movement velocity of the left ventricular base decreased just after adrenaline infusion, remained low after 1 week, and recovered to near-baseline levels after 3-4 weeks in group L. Unique cardiac lesions identified by deposits of carbon particles were frequently observed on the left ventricular basal portion, almost always associated with the mitral valve and papillary muscles, but were never observed in the apical area. Lesions involving all areas of the left ventricular basal portion were observed in 22 of 23 animals in group L, but in only 2 of 15 animals in group S. Basal cardiomyopathy developed in rabbits with ventricular tachycardias induced by a single injection of adrenaline.

[A case of nonarteritic anterior ischemic optic neuropathy with hypertension, diabetes mellitus, hyperlipidemia and severe stenosis of the internal carotid artery].

A 76 year-old man had had hypertension, diabetes mellitus and hyperlipidemia since 1985, and bruit in his left neck since 1993. He had abrupt decrease in left visual acuity on November 24, 2005, and visited an ophthalmologist. On November 28, his corrected visual acuity was 1.0 in the right and 0.1 in the left. The examination of optic fundi showed ear-side edema of the left optic disk. Fluorescence examination of the left optic fundus showed delay in early filling and later hyperfluorescence. Goldman visual field examination showed horizontal lower semiblindness. Since he did not complain of eye pain, his blood examination showed no reaction of inflammation, and he had hypertension, diabetes mellitus and hyperlipidemia, anterior ischemic optic neuropathy was diagnosed. The treatment with aspirin, alprostadil and prednisolone transiently improved the optic fundi and visual acuity, but his left visual acuity returned to 0.1. Carotid ultrasonography showed 95 percent stenosis in the left internal carotid artery. As there is no established treatment for ischemic optic neuropathy, the management of risk factors is most important.

Ventricular tachyarrhythmia-related basal cardiomyopathy in rabbits with vagal stimulation--a novel experimental model for inverted Takotsubo-like cardiomyopathy.

BACKGROUND: Electrical stimulation of the intact (unsectioned) cervical vagus in rabbits frequently provokes ventricular tachyarrhythmias that are often accompanied by mitral regurgitation. Unique pathological lesions often arise on the mitral valve, papillary muscles, and mitral annulus (mitral complex), the latter two of which become swollen and stiffened. These lesions are reversible in nature. Previous studies have essentially ignored the basal portion except for the mitral annulus. Therefore, the present study examined pathological lesions on the left ventricular basal portion in rabbits. METHODS: The intact right vagal nerves of 20 anesthetized rabbits were repeatedly electrically stimulated under electrocardiographic monitoring. Colloidal carbon (lml) was injected intravenously immediately after the end of the stimulation and all animals were killed 1 week later. Pathological lesions were identified as carbon deposits visible at gross examination. RESULTS: Ventricular bigeminy was induced after vagal stimulation in 15 (75%) of the 20 rabbits. Pathological lesions were evident on the basal portion in 16 (80%) and on the mitral valve and papillary muscles of 15 (75%) of the 20 rabbits. Ventricular bigeminy was closely associated with the development of the pathological lesions, which were rarely observed on the ventricular apex. CONCLUSION: Cardiomyopathic lesions involving the basal portion and mitral complex were frequently induced in rabbits by vagal stimulation. These lesions bear a close similarity in distribution and reversibility to inverted Takotsubo cardiomyopathy.

Left bundle branch block with intermittent QRS axis switching: observation of a hypertensive patient for 18 years.

A 64-year-old man who had been prescribed antihypertensive drugs since 1971 attended our clinic in 1988 with hypertension and electrocardiographic abnormalities. An electrocardiogram revealed left axis deviation (LAD) in 1988 and slightly prolonged PQ intervals in 1993. Complete left bundle branch block (CLBBB) with LAD developed in May 1995. The wide QRS of the CLBBB had never returned to the normal narrow QRS and had intermittently alternated between LAD and normal axis. The PQ intervals were longer when the QRS axis showed LAD compared to that with normal QRS axis. The QRS complexes in leads V1-V3 revealed an R wave at LAD and a QS pattern at normal axis. During a deep breathing test, the QRS axis switched from normal axis to LAD at the end of forced expiration and also switched from normal axis to LAD within a few minutes after the exercise test. These results suggest that the shift of the QRS axis might be related to the tone of the autonomic nervous system.

Effects of aging and sex on progression of carotid intima-media thickness: a retrospective 6-year follow-up study.

AIM: We retrospectively examined the relationship of aging, sex and risk factors to increased carotid intima-media thickness (IMT) over a follow-up period of 6 years in patients with multiple risk factors. METHODS: Subjects were comprised of 463 patients (287 men, 176 women) with a mean age of 64 +/- 0.4 years who had undergone carotid ultrasonography twice or more at intervals of 5 years or older. The mean follow-up period was 6.0 +/- 0.1 years. RESULTS: Mean baseline IMT for all subjects was 1.40 +/- 0.02 mm, and no significant difference was seen between sexes. Mean IMT after 6 years for all subjects was 1.84 +/- 0.03 mm, and was significantly greater in men than in women. Mean annual increase in IMT (Delta IMT) for all subjects was 0.073 +/- 0.005 mm/year, with a significant positive correlation between baseline age and Delta IMT (r = 0.11, P < 0.05), and Delta IMT was significantly greater in men than in women (0.087 +/- 0.007 mm vs 0.050 +/- 0.007 mm, P < 0.001). IMT increased with age in both men and women, but Delta IMT increased with age only in men. Multivariate analysis showed baseline age and diabetes mellitus as significant risk factors with baseline IMT as the objective variable. Age and sex represented significant risk factors with DeltaIMT as the objective variable. CONCLUSION: Sex differences exist in the relationship between increases in IMT and age. Age, sex and diabetes mellitus represented the main risk factors.

Marked reversible ST-T abnormalities induced by cardiac compression from a retrosternal gastric tube used to reconstruct the esophagus after tumor resection. A case of a diabetic patient and mini-review of 7 reported patients.

A 69-year-old male patient with type 1 diabetes mellitus had been under treatment at our outpatient clinic since the age of 65. He had previously undergone surgery for esophageal cancer at the age of 55; the excised portion of the esophagus was replaced by a retrosternal gastric tube. He was admitted to our hospital for suspected pneumonia on April 8, 2004. An electrocardiogram (ECG) on admission showed marked ST depression in leads V1 and V2, and prominent negative T waves in leads I and aVL; however, the T waves unexpectedly flattened after 2 minutes and the ST depression resolved after about 4 hours. On January 7, 2005, we performed a deep breathing test to analyze the effects of movements of the thoracic wall and intrathoracic structures on the ECG. In this test, deep inspiration induced ST depression reaching 0.5 mV in leads V1 to V3; this resolved on switching to deep expiration. ECG changes together with chest computed tomography images supported the concept that the ST-T abnormalities were induced by cardiac compression caused by expansion of the gastric tube between the sternum and heart. We have reviewed 7 other similar reported cases.