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Notes: Objective: The purpose of this study was to investigate how the modulation of electrical microvolt level T-wave alternans (Twa) relates to left ventricular late potentials as evaluated by heart rate variability (HRV), QT dispersion, and plasma catecholamine levels.Background: The Twa and left ventricular late potentials are promising noninvasive powerful markers for risk prediction in patients with ischemic heart disease (IHD) and/or cardiomyopathy. However, their relation to autonomic activity is unclear.Methods: In 56 patients with stable IHD-measured Twa at rest and during controlled bicycle ergometer testing, we simultaneously recorded recent noninvasive electrocardiographic approaches, such as HRV, QT dispersion, and left ventricular late potentials. Plasma norepinephrine (NE) and epinephrine (E) were also measured.Results: (1) There were no significant differences in clinical findings, NE, and E levels between positive (group A) and negative (group B) Twa. Left ventricular late potentials, LF (low frequency spectra), as well as HF (high frequency spectra) in group A were significantly lower than in group B, but LF/HF did not differ significantly between the two groups. There was a significant inverse correlation between Twa microvoltage and LF/HF that was higher during exercise (r = -0.51, P = 0.006) than at rest (r = -0.34, P 〈 0.01). (2) There were no significant differences in clinical findings between positive (group C) and negative (group D) left ventricular late potentials. Plasma NE in group C was significantly higher than in group D (1060 ± 429 pg/mL vs 395 ± 219, P 〈 0.05). Furthermore, LF/HF in group C was significantly lower than in group D (0.96 ± 0.27 vs 1.1 ± 0.11, P 〈 0.05). There were no significant correlations between left ventricular late potential parameters and QT or QTc dispersion.Conclusions: The Twa microvoltage in patients with stable IHD exhibits similar physiologic conditions as in patients with lower HRV indices. The presence of left ventricular late potentials might be affected by sympathetic nerve modulation.

Notes: Anginal pain perception has been reported to be modulated by endogenous opiates, or peripherally as a result of neuropathy. However, whether these factors can contribute to the mechanisms of silent myocardial ischemia remains unclear.〈section xml:id="abs1-2"〉〈title type="main"〉MethodsBased on the results of previous exercise testing, a total of 140 patients (39 diabetic and 101 nondiabetic) with exercise-induced myocardial ischemia were divided into the following four groups: 19 diabetics with silent myocardial ischemia; 49 nondiabetics with silent myocardial ischemia; 20 diabetics with anginal symptoms; and 52 nondiabetics with anginal symptoms. All patients underwent treadmill exercise testing and 24-hour ambulatory electrocardiographic recording. Plasma beta-endorphin levels and tactile thresholds were measured before and during exercise. With regard to the ambulatory electrocardiographic recording, the mean of the standard deviations (SDNNIDX) of all normal sinus RR intervals during successive 5-minute recording periods over 24 hours was analyzed and considered as an index of the autonomic function.〈section xml:id="abs1-3"〉〈title type="main"〉ResultsThe plasma beta-endorphin level during exercise was significantly greater in nondiabetic patients with silent myocardial ischemia than in diabetics with silent myocardial ischemia and in nondiabetics with anginal symptoms. The SDNNIDX mean was significantly less in diabetics with silent myocardial ischemia than in diabetics with anginal symptoms; in nondiabetics with anginal symptoms; and in nondiabetics with silent myocardial ischemia.〈section xml:id="abs1-4"〉〈title type="main"〉ConclusionsWe confirm that elevated beta-endorphin levels are associated with silent myocardial ischemia in nondiabetic patients and that abnormalities in autonomic function seen in diabetes are associated with the silent form of myocardial ischemia. A.N.E. 1997;2(4):319–325

Notes: Isoproterenol-Induced vs Nitroglycerin-Induced Syncope. Introduction: A reduction in left ventricular volume and an increase in epinephrine levels have been reported in tilt-induced neurally mediated syncope. To compare the mechanisms of isoproterenol-induced and nitroglycerin-induced syncope during head-up tilt and to investigate the role of catecholamines, the temporal changes in plasma levels of norepinephrine and epinephrine and in left ventricular volume were measured. Methods and Results: The first study population consisted of 90 patients with syncope of unknown etiology and 12 control subjects. The second study population consisted of 43 patients with unexplained syncope. In the first study, head-up tilt (80° angle) was conducted for 40 minutes, and norepinephrine and epinephrine levels were measured. In the second study, all patients were randomly allocated to either isoproterenol test (20 patients) or nitroglycerin test (23 patients) for 20-minute head-up tilt. Isoproterenol infusion was given at a rate of 1 to 3 μ g/min. Intravenous infusion of nitroglycerin was started at 250 μ g/hour with increasing dosages up to 1,500 μ g/hour. Norepinephrine and epinephrine were measured in peripheral venous blood. Left ventricular volumes were measured by echocardiography with patients in the supine position and during head-up tilt every 1 minute. End-diastolic volume and end-systolic volume were calculated. In the first study, 61 patients demonstrated a positive response and 29 patients demonstrated a negative response. Plasma norepinephrine changes during head-up tilt were not significantly different, whereas epinephrine levels were significantly higher in the positive patients than in the negative and control subjects (148 ± 118 pg/mL vs 66 ± 31 pg/mL and 55 ± 27 pg/mL). Thirteen of the 20 patients given isoproterenol and 15 of the 23 patients given nitroglycerin showed a positive head-up tilt (65.0% vs 65.2%; P = NS). During isoproterenol and nitroglycerin infusion head-up tilt, epinephrine in the positive group determined by the nitroglycerin test was significantly higher than that in the other three groups (103 ± 38 pg/mL vs 60 ± 33 pg/mL, 31 ± 21 pg/mL, and 50 ± 52 pg/mL). In contrast, end-systolic volume was significantly smaller in the positive group than in the other three groups based on findings of the isoproterenol test. Conclusion: The findings suggest that nitroglycerin triggers head-up tilt-induced syncope by increasing epinephrine levels, whereas isoproterenol induces syncope by decreasing left ventricular volume.

Notes: Application of ultraviolet light irradiation to a photocrosslinkable chitosan (Az-CH-LA) aqueous solution including fibroblast growth factor-2 (FGF-2) results within 30 seconds in an insoluble, flexible hydrogel. The FGF-2 molecules retained in the chitosan hydrogel remain biologically active and are released from the chitosan hydrogel upon in vivo biodegradation of the hydrogel. To evaluate the accelerating effect on wound healing of this hydrogel, full-thickness skin incisions were made in the backs of healing-impaired diabetic (db/db) mice and their normal (db/+) littermates. The mice were later killed, and histological sections of the wound were prepared. The degree of wound healing was evaluated using several histological parameters such as the rate of contraction, epithelialization, and tissue filling. Application of the chitosan hydrogel significantly advanced the rate of contraction on Days 0 to 2 in db/db and db/+ mice. Although the addition of FGF-2 into the chitosan hydrogel in db/+ mice had little effect, application of the chitosan hydrogel–containing FGF-2 further accelerated the adjusted tissue filling rate (Days 2 to 4 and Days 4 to 8) in db/db mice. Furthermore, the chitosan hydrogel–containing FGF-2 markedly increased the number of CD-34-positive vessels in the wound areas of db/db mice on Day 4. Thus, the application of chitosan hydrogel–containing FGF-2 onto a healing-impaired wound induces significant wound contraction and accelerates wound closure and healing.