A reduction in hospital admissions for acute coronary syndromes (ACS) has been observed globally in the aftermath of the pneumonia outbreak caused by coronavirus disease 2019 . 1 Despite emergence of anecdotal reports, formal evaluation of variation in percutaneous coronary intervention (PCI) rates during the COVID-19 outbreak has not yet been reported. Italy is one of the countries most heavily affected by the COVID-19 pandemic with 168,941 confirmed cases and 22,170 deaths as of April 5, 2020.We investigated the association between the outbreak of COVID-19 and PCI rates for ACS in the Campania region, which with 5.8 million residents represents about 10% of the Italian population. Data were obtained from 20 out of 21 PCI centers over an 8-week period, including 4-week before and 4-week after the COVID-19 outbreak corresponding with the first reported case declared by the Civil Protection Department on February 27, 2020. Incidence rates and their ratios were calculated using Poisson regression analysis and interactions for gender and age were estimated by adding the interaction term to the regression models. 2 Population denominators, which were used as offset, were obtained from the Italian census. The ratio change in PCI rates for the entire 8-week interval was estimated by adding a linear term to the Poisson regression. The study was approved by the Ethics Committee of the University of Naples Federico II (Naples, Italy).From January 30, 2020 to March 26, 2020, a total of 1,831 PCIs were performed in the Campania region; of them 738 (40.31%) were elective PCI (not included), 604 (32.99%) PCI for non-ST-segment elevation acute ACS (NSTE-ACS), and 489 (26.71%) PCI for ST-segment elevation myocardial infarction (STEMI). Mean age was 65.7 years (standard deviation 12), and 804/1,093 PCIs (73.56%) were performed in men. There were no differences in mean age
BACKGROUND Heart period variability provides useful prognostic information on autonomic cardiac control, and a strong association has been demonstrated after myocardial infarction (MI) between cardiac mortality, sudden death, and reduced total power, ultralow-frequency (ULF) power, and very-low-frequency (VLF) power. Converting enzyme inhibitors are widely used in MI patients, but their influence on heart period variability remains to be defined. METHODS AND RESULTS Time- and frequency-domain measures of heart period variability were calculated from 24-hour Holter monitoring in 40 patients with a first uncomplicated MI. After baseline examination between 48 and 72 hours after symptom onset, patients were randomly assigned to placebo or captopril administration, and on the third day, 24-hour Holter monitoring was repeated. No changes in time and frequency domain were detectable after placebo. After captopril, the SD of all normal RR (NN) intervals (SDNN) increased from 90 +/- 29 to 105 +/- 30 milliseconds (P < .01); the SD of the average NN intervals for all 5-minute segments (SDANN index) and the mean of the SDs of all NN intervals for all 5-minute segments (SDNN index) also increased from 74 +/- 24 to 90 +/- 26 milliseconds (P < .01) and from 45 +/- 17 to 49 +/- 15 milliseconds (P < .05), respectively. The root mean square successive difference (r-MSSD) and the percent of differences between adjacent NN intervals > 50 milliseconds (pNN50) remained unchanged. In regard to frequency-domain measures, after captopril, total power (ln unit) increased from 8.28 +/- 0.42 to 8.47 +/- 0.30 (P < .01); considering the frequency bands, a significant increase was observed in ULF (P < .01), VLF (P < .05), and low-frequency (LF) power (P < .05), whereas high-frequency (HF) power remained unchanged. CONCLUSIONS This study supports the hypothesis that the renin-angiotensin system modulates the amplitude of ULF and VLF power. Furthermore, it demonstrates that in MI patients, converting enzyme inhibition favorably modifies measures of heart period variability strongly associated with a poor prognosis.
This study aimed to characterize sympathovagal balance by heart period power spectrum analysis in hypertensive patients with echocardiographic evidence of left ventricular hypertrophy. Twenty ambulatory patients (11 men and 9 women), aged 50 +/- 10 years, with established essential hypertension and echocardiographic left ventricular hypertrophy, performed 24-h blood pressure monitoring and electrocardiogram Holter recording on 2 consecutive days. Twenty age- and sex-matched normal subjects comprised the control group. Power spectrum analysis, performed using the fast Fourier transform algorithm, demonstrated lower values of low and high frequency power in hypertensives than in controls, while ultralow and very low frequency power were similar in the two groups. Very low frequency, low frequency, and high frequency power increased during the night in both groups, showing a similar circadian pattern. We found a direct correlation between daytime systolic (r = 0.51; P < .05) and diastolic (r = 0.52; P < .05) blood pressure and left ventricular mass index. Moreover, negative correlations were found between left ventricular mass index and low frequency (r = -0.47; P < .05) and high frequency power (r = -0.47; P < .05). There was a direct correlation between nighttime decrease in systolic blood pressure and nighttime increase in high frequency power (r = 0.45; P < .05). As 24-h low frequency and high frequency power, obtained using the Fourier transform algorithm, both reflect the parasympathetic modulation of heart rate, our results demonstrate that hypertensive patients with left ventricular hypertrophy are characterized by a sympathovagal imbalance with a reduction of vagal tone that is more evident with increasing severity of hypertension.
In this study we evaluated in hypertensive patients the effects of drug-induced left ventricular hypertrophy regression on cardiac autonomic control, as assessed by means of heart period variability analysis. Power spectral analysis of 24-hour electrocardiographic monitoring was performed in 30 hypertensive patients with left ventricular hypertrophy at baseline, after 1 year of lisinopril treatment, and after 1 month of drug withdrawal. At the same times, patients underwent 24-hour blood pressure monitoring, echocardiographic study, and plasma renin activity assessment. Lisinopril treatment increased plasma renin activity and reduced 24-hour systolic and diastolic pressures (from 159 +/- 14 to 121 +/- 8 and from 103 +/- 7 to 80 +/- 3 mm Hg, respectively) and left ventricular mass index (from 159 +/- 33 to 134 +/- 26 g/m2); moreover, in 12 of 30 patients, left ventricular mass normalization was achieved. Drug withdrawal was followed by an increase in blood pressure without left ventricular mass modification. In the total study population, only high-frequency power was higher after lisinopril treatment. In the subgroup of patients with left ventricular mass normalization, daytime and nighttime high-frequency powers as well as nighttime total and very-low-frequency powers were higher after 1 year of treatment than at baseline. In the remaining 18 patients, power spectral measures after treatment were slightly lower than at baseline and were even lower after drug withdrawal. Thus, in hypertensive hypertrophic patients, lisinopril treatment improves sympathovagal imbalance when left ventricular mass normalization is achieved. In patients without left ventricular mass normalization, drug withdrawal is followed by a worsening of neural cardiac control.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.