ABSTRACT
BACKGROUND: It was reported that autonomic nervous system function is altered in subjects with chronic obstructive pulmonary disease (COPD). We evaluated short- and long-term fractal exponents of heart rate variability (HRV) in COPD subjects. PATIENTS AND METHODS: We analyzed data from 30 volunteers, who were divided into two groups according to spirometric values: COPD (n = 15) and control (n = 15). For analysis of HRV indices, HRV was recorded beat by beat with the volunteers in the supine position for 30 minutes. We analyzed the linear indices in the time (SDNN [standard deviation of normal to normal] and RMSSD [root-mean square of differences]) and frequency domains (low frequency [LF], high frequency [HF], and LF/HF), and the short- and long-term fractal exponents were obtained by detrended fluctuation analysis. We considered P < 0.05 to be a significant difference. RESULTS: COPD patients presented reduced levels of all linear exponents and decreased short-term fractal exponent (alpha-1: 0.899 ± 0.18 versus 1.025 ± 0.09, P = 0.026). There was no significant difference between COPD and control groups in alpha-2 and alpha-1/alpha-2 ratio. CONCLUSION: COPD subjects present reduced short-term fractal correlation properties of HRV, which indicates that this index can be used for risk stratification, assessment of systemic disease manifestations, and therapeutic procedures to monitor those patients.
Subject(s)
Fractals , Heart Rate , Pulmonary Disease, Chronic Obstructive/physiopathology , Signal Processing, Computer-Assisted , Aged , Brazil , Case-Control Studies , Female , Heart Function Tests , Humans , Linear Models , Lung/physiopathology , Male , Middle Aged , Pulmonary Disease, Chronic Obstructive/diagnosis , Spirometry , Supine Position , Time FactorsABSTRACT
We evaluated short-term effects of sidestream cigarette smoke (SSCS) exposure on baroreflex function in spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) normotensive rats. Rats were exposed to SSCS during three weeks, 180 min, five days per week, in a concentration of carbon monoxide (CO) between 100 and 300 ppm. We observed that SSCS exposure increased tachycardic peak and heart rate range while it attenuated bradycardic reflex in WKY. In respect to SHR, SSCS also increased tachycardic peak. Taken together, our data suggests that three weeks of exposure to SSCS affects the sympathetic and parasympathetic component of the baroreflex in normotensive WKY while it tended to affect the sympathetic component in SHR.
Subject(s)
Bradycardia/physiopathology , Hypertension/physiopathology , Smoke/adverse effects , Tachycardia/physiopathology , Animals , Baroreflex , Blood Pressure/drug effects , Heart Rate/drug effects , Hypertension/drug therapy , Hypertension/pathology , Parasympathetic Nervous System/drug effects , Rats , Rats, Inbred SHR , Rats, Inbred WKY , Species Specificity , Sympathetic Nervous System/drug effectsABSTRACT
OBJECTIVES: There is a direct relationship between the regression of left ventricular hypertrophy (LVH) and a decreased risk of mortality. This investigation aimed to describe the effects of anti-hypertensive drugs on cardiac hypertrophy through a meta-analysis of the literature. METHODS: The Medline (via PubMed), Lilacs and Scielo databases were searched using the subject keywords cardiac hypertrophy, antihypertensive and mortality. We aimed to analyze the effect of anti-hypertensive drugs on ventricle hypertrophy. RESULTS: The main drugs we described were enalapril, verapamil, nifedipine, indapamina, losartan, angiotensin-converting enzyme inhibitors and atenolol. These drugs are usually used in follow up programs, however, the studies we investigated used different protocols. Enalapril (angiotensin-converting enzyme inhibitor) and verapamil (Ca(++) channel blocker) caused hypertrophy to regress in LVH rats. The effects of enalapril and nifedipine (Ca(++) channel blocker) were similar. Indapamina (diuretic) had a stronger effect than enalapril, and losartan (angiotensin II receptor type 1 (AT1) receptor antagonist) produced better results than atenolol (selective beta1 receptor antagonist) with respect to LVH regression. CONCLUSION: The anti-hypertensive drugs induced various degrees of hypertrophic regression.
Subject(s)
Antihypertensive Agents/therapeutic use , Hypertrophy, Left Ventricular/drug therapy , Animals , Humans , Hypertension/prevention & control , Hypertrophy, Left Ventricular/mortality , Rats , Remission Induction/methods , Risk Factors , Treatment OutcomeABSTRACT
OBJECTIVES: There is a direct relationship between the regression of left ventricular hypertrophy (LVH) and a decreased risk of mortality. This investigation aimed to describe the effects of anti-hypertensive drugs on cardiac hypertrophy through a meta-analysis of the literature. METHODS: The Medline (via PubMed), Lilacs and Scielo databases were searched using the subject keywords cardiac hypertrophy, antihypertensive and mortality. We aimed to analyze the effect of anti-hypertensive drugs on ventricle hypertrophy. RESULTS: The main drugs we described were enalapril, verapamil, nifedipine, indapamina, losartan, angiotensin-converting enzyme inhibitors and atenolol. These drugs are usually used in follow up programs, however, the studies we investigated used different protocols. Enalapril (angiotensin-converting enzyme inhibitor) and verapamil (Ca++ channel blocker) caused hypertrophy to regress in LVH rats. The effects of enalapril and nifedipine (Ca++ channel blocker) were similar. Indapamina (diuretic) had a stronger effect than enalapril, and losartan (angiotensin II receptor type 1 (AT1) receptor antagonist) produced better results than atenolol (selective â1 receptor antagonist) with respect to LVH regression. CONCLUSION: The anti-hypertensive drugs induced various degrees of hypertrophic regression.
