Peripheral vasodilatory dysfunction in adult patients with congenital heart disease and severely elevated pulmonary vascular resistance.

Several studies have demonstrated that pulmonary vascular abnormalities precede alterations in aortic circulation downstream in animal models of heart failure. The relationship between increased pulmonary vascular resistance (PVR) and agonist-induced limb vasodilatory response remains unknown in patients with congenital cardiovascular shunt lesions (CSL). The authors hypothesized that patients with CSL and severely elevated PVR will show a defective vasomotor response in the peripheral vascular bed. To examine this hypothesis we measured forearm blood flow (FBF) responses to the endothelium-dependent vasodilator acetylcholine and the endothelium-independent vasodilator sodium nitroprusside. The values for these FBF responses were compared with PVR in adult patients with CSL (n=20) and healthy age- and sex-matched controls (n = 15). When patients with CSL were divided into 2 subgroups by median value of PVR, in the lower PVR subgroup, acetylcholine-induced FBF changes were selectively and significantly lower than in the healthy control group (p <0.05). In the higher PVR subgroup, FBF responses to both acetylcholine and sodium nitroprusside were significantly blunted compared to healthy controls (both p < 0.01). In addition, when FBF changes above baseline for each dose of acetylcholine and sodium nitroprusside were cumulated and used as acetylcholine response and sodium nitroprusside response, the sensitivity and specificity for identifying patients with Eisenmenger's type of CSL was 100% and 80% by acetylcholine response, and 67% and 80% by sodium nitroprusside response, respectively. In conclusion, adult CSL patients with elevated PVR and severe pulmonary arterial hypertension showed generalized vasodilator dysfunction in the forearm vasculature. This result suggests that upper limb resistance vessel dysfunction may be an indicator for advanced stage of adult patients with CSL.

A case of ventricular asystole without escape rhythm 4 days after percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy with drug-resistant paroxysmal atrial fibrillation.

A 42-year-old man with a more than 10-year history of hypertrophic obstructive cardiomyopathy, but no history of heart failure or syncope, had left ventricular outflow tract pressure gradient (LVOT-PG) of 50-80 mmHg on Doppler echocardiography. In June 2010, he experienced general malaise on effort, and LVOT-PG increased to 124 mmHg. Two months later, he suffered a transient ischemic attack, complicated with atrial fibrillation (AF). He underwent cardiac defibrillation and was prescribed amiodarone, but the arrhythmia recurred easily. Therefore, percutaneous transluminal septal myocardial ablation (PTSMA) was performed to prevent AF. The procedure entailed transient complete atrioventricular block (CAVB), which was resolved after a few hours. Four days later, CAVB recurred and advanced to fatal ventricular asystole without escape rhythm. The patient was resuscitated instantaneously and recovered without brain damage. Finally, a DDD permanent pacemaker was implanted 10 days after the procedure. Except for conduction problems, his cardiac condition was good after PTSMA, as paroxysmal AF disappeared and LVOT-PG was markedly decreased. CAVB is a well-known complication of PTSMA, but fatal ventricular asystole several days after the procedure is rare. Intensive care is required after PTSMA implementation.

Association of decreased variation of R-R interval and elevated serum C-reactive protein level in a general population in Japan.

Several studies have suggested that an increased high sensitivity C-reactive protein (hsCRP) level is a strong independent predictor of increased risk for atherosclerotic cardiovascular mortality and morbidity. Reduced heart rate variability (HRV) has also been reported to predict cardiovascular events such as sudden death and myocardial infarction in apparently healthy subjects. The aim of this cross-sectional study was to test the possible correlation between variation of the R-R interval as one of the markers of HRV and serum hsCRP levels in a general population in Japan. Resting, supine, 2-minute, beat-to-beat heart rate data were collected in 823 randomly selected participants enrolled in our cohort study. The coefficient of variation of the R-R interval (CVrr) was obtained as a parameter of HRV. To determine which factors predict the presence of low CVrr (below the 5 percentile) in this group, we performed a multivariate logistic regression analysis using cardiovascular risk factors and an elevated hsCRP level as independent variables. The lowest CVrr group showed significantly higher hsCRP levels compared to those of other quartiles (P < 0.01). After adjustment for confounding factors such as age, heart rate, obesity, hypercholesterolemia, and hypertension by multivariate logistic analysis, an elevated hsCRP level (OR = 3.11, 95%CI; 1.27-7.60: P < 0.02) was a significant independent predictor of low CVrr. The results of the present study indicate that an increased serum hsCRP level is significantly associated with reduced CVrr in this general population. It is conceivable that the parasympathetic nerve withdrawal and inflammation could interact with each other, resulting in the progression of atherosclerotic cardiovascular disease.

[Atypical takotsubo cardiomyopathy with preservation of apical contraction: a case report including pathological findings].

A 60-year-old woman presented with sudden chest and back pain. Electrocardiography suggested anterior myocardial infarction but coronary angiography revealed no significant stenosis in the coronary artery. Left ventriculography revealed akinesis of the mid ventricle and preserved contraction of the apical wall. The clinical condition of atypical left ventricular akinesia was suggested to be the same as conventionally reported typical takotsubo cardiomyopathy. Repeated left ventriculography revealed the abnormal wall motion had disappeared. The findings of endomyocardial biopsy were compatible with takotsubo cardiomyopathy. Although the clinical presentation of the left ventricle is atypical, the pathological findings may be the same as typical takatsubo cardiomyopathy.

Muscle metaboreflex is blunted with reduced vascular resistance response of nonexercised limb in patients with chronic heart failure.

BACKGROUND: Exercise-mediated muscle metaboreflex (MMR) activates the sympathetic nervous system afferently and may play an important role in the reduction in blood flow in nonexercised limb, thus enhancing exercised skeletal muscle blood flow (ie, normal regional blood flow redistribution during exercise). However, few data are available to describe the relationship between MMR and peripheral vascular control during exercise in congestive heart failure (CHF). The aim of this study was to determine whether MMR is impaired in CHF, and, if so, whether MMR is related to clinical severity of CHF and to changes in nonexercised limb vascular resistance in CHF. METHODS AND RESULTS: Eleven CHF patients and 9 healthy age- and gender-matched controls were examined. All subjects performed a rhythmic handgrip exercise test at 50% of maximal voluntary contraction for 3 minutes on 2 occasions with and without postexercise upper arm regional circulatory occlusion (RCO/non-RCO). Changes in systolic blood pressure were measured and plotted against protocol time for both RCO and non-RCO. The area under each curve was estimated, and the calculating difference in the area between RCO and non-RCO was regarded as MMR. In addition, changes in calf vascular resistance were measured continuously by plethysmography after the handgrip test and the area differences between the RCO and non-RCO data was taken to represent MMR-provoked resistance changes in the nonexercised limb. During the handgrip exercise, systolic blood pressure increased similarly on the 2 occasions for both groups. MMR was significantly lower in CHF patients than in controls (68.2 +/- 23.1 versus 160.4 +/- 29.6 arbitrary units; P < .05). Decrease in MMR activity was related to clinical severity of CHF (controls, 160.4 +/- 29.6; New York Heart Association class II, 87.6 +/- 29.8; New York Heart Association class III, 34.3 +/- 34.8 arbitrary units; P < .05). The increase in calf vascular resistance between RCO and non-RCO protocols in the control group was significant (+146.5 +/- 38.0 arbitrary units; P < .05), whereas the difference in the CHF group was not significant (-72.9 +/- 126.9 arbitrary units; not significant). CONCLUSIONS: Exercise-induced MMR control in mild to moderate CHF is impaired in association with a blunted increase in nonexercised limb vascular resistance. This suggests that blunted MMR activity impairs regional blood flow redistribution and may contribute in part to exercise intolerance in this disorder.