[show abstract][hide abstract] ABSTRACT: Compression of the trachea, bronchi, and pulmonary arteries are complications in patients with large thoracic aortic aneurysms. In this case, we report unexpected cardiopulmonary collapse manifested by general anesthesia before surgery in an asymptomatic patient with a large thoracic aortic aneurysm.
We present the case of a 32-year-old man with a 10-cm aneurysm in the ascending aorta. A total aortic arch replacement was planned. After intravenous anesthesia, his aneurysm occluded the left main bronchus and right pulmonary artery simultaneously, and induced severe hypoxia. Percutaneous cardiopulmonary support was conducted and the patient recovered from cardiopulmonary collapse successfully. After the patient regained consciousness from anesthesia, the findings of organ compressions disappeared. At the second surgery, percutaneous cardiopulmonary support was initiated with local anesthesia before general anesthesia and intubation. The operation was performed successfully without any adverse events.
We experienced a case of hemodynamic collapse induced by general anesthesia in a patient of an unruptured thoracic aortic aneurysm. It is important to recognize that fatal organ compression might be caused by general anesthesia even in asymptomatic patients with thoracic aortic aneurysm.
[show abstract][hide abstract] ABSTRACT: Atrial fibrillation (AF) is a common complication in heart failure (HF) patients. However, it remains unclear whether irregular ventricular response patterns induced by AF increase sympathetic nerve activity. We measured resting multi- and single-unit muscle sympathetic nerve activity (MSNA) in 21 age-matched HF patients with chronic AF (n = 11) rhythm or sinus rhythm (SR, n = 10). The multi-unit MSNA, which was expressed as total activity, was similar between HF + AF patients and HF + SR patients. However, the single-unit MSNA in HF + AF patients was significantly greater than that in HF + SR patients (62 ± 9 spikes min(-1) vs. 42 ± 4 spikes min(-1), P < 0.05). Moreover, the incidence of multiple firing of single-unit MSNA within a given burst was augmented in HF + AF patients as compared with HF + SR patients (48 ± 8% vs. 26 ± 3%, P < 0.01). A significant negative relationship was observed between the reduced diastolic pressure induced by a prolonged cardiac interval in AF subjects and single-unit MSNA frequency within one cardiac interval in each HF + AF subject. The firing characteristics of single-unit MSNA were different between HF patients with AF and HF patients with SR; particularly, those with a prolonged long RR interval showed multiple firings of single-unit MSNA. These findings suggest that AF per se leads to the instantaneous augmentation of single-unit MSNA induced by decreased diastolic pressure, which might partially contribute to disease progression in HF patients.
The Journal of Physiology 12/2011; 590(Pt 3):509-18. · 4.38 Impact Factor
[show abstract][hide abstract] ABSTRACT: Aldosterone is implicated in the pathogenesis of several cardiovascular diseases, including ischemia reperfusion (I/R) and myocardial infarction, and also causes oxidative stress and inflammation in cardiovascular systems. Benidipine, a long-acting T- and L-type calcium channel blocker, reduces infarct size following myocardial I/R in rabbits. Benidipine also inhibits the production of aldosterone in vitro. However, the precise mechanism of this phenomenon in vivo remains unknown. We therefore evaluated whether benedipine has a beneficial role through the regulation of oxidative stress in myocardial I/R. C57BL/6J mice were subjected to 30 min of left ascending coronary I/R. Benidipine was administered orally at 3 mg kg(-1) daily for 3 weeks without any changes in hemodynamic variables. Benidipine significantly reduced infarction size (13.4±2.5%) compared with controls (25.5±3.6%). Urinary 8-hydroxy-2' deoxyguanosine (8-OHdG), a marker of oxidative DNA damage, increased significantly after I/R. I/R induced increases in 8-OHdG were significantly lower with benidipine. Local myocardial 8-OHdG was also elevated in I/R, but this augmentation was significantly suppressed with benidipine. The plasma aldosterone concentration (PAC) significantly increased 2 days after I/R and remained elevated at least 7 days after I/R. Treatment with benidipine significantly decreased I/R-induced elevation of the PAC. I/R-induced markers of fibrosis in hearts also reduced in benidipine. These results suggest that the administration of benidipine reduces myocardial infarct size as well as systemic oxidative stress after I/R. These phenomena are partially linked to reduced plasma aldosterone levels.
Hypertension Research 11/2011; 35(3):287-94. · 2.79 Impact Factor
[show abstract][hide abstract] ABSTRACT: Activation of the sympathetic nervous system is augmented in patients with type 2 diabetes mellitus (DM). Pioglitazone, an anti-diabetic drug, improves insulin resistance, but its influence on sympathetic nerve activity is not clear. To identify the relationship between insulin resistance and sympathetic activity, we examined muscle sympathetic nerve activity (MSNA) in controlled type 2 DM patients with alpha-glucosidase inhibitor (GI). We measured MSNA and calculated homeostasis model assessment of insulin resistance index (HOMA-IR) in twelve DM patients treated with alpha-GI and thirteen age-matched healthy subjects. In DM patients with alpha-GI, all parameters were reexamined after three months of treatment with pioglitazone. MSNA and HOMA-IR were significantly greater in DM patients with alpha-GI compared to healthy subjects. Hemoglobin A1c did not differ in DM patients before and after pioglitazone. However, pioglitazone significantly decreased MSNA in DM patients compared with alpha-GI (21.7±5.2 vs. 32.0±6.8 burst/min, p<0.01). Furthermore, MSNA level in pioglitazone was similar to that in healthy subjects. HOMA-IR significantly decreased after pioglitazone, and a significant relationship was found between the absolute change in MSNA and HOMA-IR (r=0.65, p<0.05). These results suggest that improved insulin resistance with pioglitazone provides an additional effect on inhibition of sympathetic nerve activity.
[show abstract][hide abstract] ABSTRACT: Sympathetic activation in chronic heart failure (CHF) is greatly augmented at rest but the response to exercise remains controversial. We previously demonstrated that single-unit muscle sympathetic nerve activity (MSNA) provides a more detailed description of the sympathetic response to physiological stress than multi-unit nerve recordings. The purpose of this study was to determine whether the reflex response and discharge properties of single-unit MSNA are altered during handgrip exercise (HG, 30% of maximum voluntary contraction for 3 min) in CHF patients (New York Heart Association functional class II or III, n = 16) compared with age-matched healthy control subjects (n = 13). At rest, both single-unit and multi-unit indices of sympathetic outflow were augmented in CHF compared with controls (P < 0.05). However, the percentage of cardiac intervals that contained one, two, three or four single-unit spikes were not different between the groups. Compared to the control group, HG elicited a larger increase in multi-unit total MSNA (Delta1002 +/- 50 compared with Delta636 +/- 76 units min(-1), P < 0.05) and single-unit MSNA spike incidence (Delta27 +/- 5 compared with Delta8 +/- 2 spikes (100 heart beats)(-1)), P < 0.01) in the CHF patients. More importantly, the percentage of cardiac intervals that contained two or three single-unit spikes was increased (P < 0.05) during exercise in the CHF group only (Delta8 +/- 2% and Delta5 +/- 1% for two and three spikes, respectively). These results suggest that the larger multi-unit total MSNA response observed during HG in CHF is brought about in part by an increase in the probability of multiple firing of single-unit sympathetic neurones.
The Journal of Physiology 04/2009; 587(Pt 11):2613-22. · 4.38 Impact Factor
[show abstract][hide abstract] ABSTRACT: The number of the elderly patients with atrial fibrillation (AF) is increasing, but the current status of anticoagulation therapy for elderly patients with AF in Japan is not clear.
Among the patients registered in the "Hokuriku Atrial Fibrillation Trial (HAT) 1", 365 AF patients aged > or =65 years were enrolled in this study. Warfarin was used for significantly less patients in the oldest group aged > or =85 years (36%) than in younger populations, but the percentage of antiplatelet use in this oldest population was largest (40%). The elderly group (> or =85 years) was compared with a younger group aged between 75 and 84 years. Warfarin was given to 61% of the younger group compared with 36% in the elderly group. In the younger group, the more thromboembolic risks they had according to CHADS2 score, the more warfarin was used, whereas there was no clear trend in the usage of warfarin in the elderly group.
The number of elderly Japanese patients with AF taking warfarin is currently low, but because the population of elderly AF patients will increase in the future, there is a need for safe and suitable anticoagulation therapy for elderly patients.
[show abstract][hide abstract] ABSTRACT: In order to determine the effect of pimobendan on sympathetic nerve activity and cardiopulmonary baroreflex (CPB), electrocardiogram, direct arterial pressure, central venous pressure (CVP) and cardiac output were recorded along with muscle sympathetic nerve activity (MSNA) in 8 healthy young men. CPB function was evaluated before and 60 min after oral administration of 5 mg pimobendan using the response of MSNA to lower body negative pressure (LBNP) of -5 and -10 mm Hg. The same protocol also was performed during handgrip exercise. Cardiac index, MSNA increased and CVP decreased significantly (p<0.01, respectively), but arterial pressure and heart rate unchanged after pimobendan administration. During LBNP, CVP decreased and MSNA increased significantly. CPB sensitivity was augmented from 5.53+/-0.75 to 8.59+/-0.78 burst incidence/mm Hg after pimobendan administration (p<0.01). Pimobendan did not alter the percentage increase of MSNA during handgrip exercise. In conclusion, pimobendan induces an increase in basal sympathetic nerve activity by decreasing CVP and augmenting CPB sensitivity without changing arterial pressure in healthy young men.
[show abstract][hide abstract] ABSTRACT: The aim of this study was to: (1) evaluate atrial electromechanical coupling using M-mode Doppler tissue; and (2) test its clinical impact for detecting atrial abnormalities in paroxysmal atrial fibrillation (AF). Using Doppler tissue, the time intervals from the onset of P wave until the backward motions of the right and left atrioventricular rings in the apical 4-chamber view corresponding to the atrial contractions were measured. In paroxysmal AF group, these intervals were significantly longer than in the control group. Using the criteria that an abnormal time interval from the onset of P wave until the backward motion of the left atrioventricular ring is longer than 112 milliseconds, the sensitivity, the specificity, and the positive predictive values for paroxysmal AF are 73%, 93%, and 93%, respectively. This parameter is affected in patients with paroxysmal AF and should be useful for detecting atrial impairment related to paroxysmal AF.
Journal of the American Society of Echocardiography 02/2005; 18(1):39-44. · 4.28 Impact Factor
[show abstract][hide abstract] ABSTRACT: Introduction: The Rho/Rho-kinase pathway has been related to various physiological responses of the cardiovascular system. Previous reports have suggested a significant effect of Rho signals on the electrophysiological characteristics of the heart. We hypothesized that the Rho/Rho-kinase system would contribute to the rapid pacing-related change of atrial effective refractory period (AERP).Methods and Results: In 17 dogs, AERP was measured at the right atrial appendage (RAA) and posterior left atrium (LA) before, during, and after 6-hours rapid atrial pacing at 500 bpm. Saline control (n = 5), verapamil (n = 5), or fasudil (n = 7) were infused throughout the protocol. The shortening of AERP after rapid pacing was abrogated by the administration of verapamil, as reported in previous studies. Furthermore, fasudil (Rho/Rho-kinase inhibitor) influenced the change of AERP in a manner similar to the infusion of verapamil throughout the experiments.Conclusions: Since the AERP was attenuated by fasudil, rapid pacing-related atrial electrophysiological changes might involve the Rho/Rho-kinase pathway.