Background and Objectives: Renal artery denervation (RDN) procedure is a broadly discussed method in the treatment of resistant hypertension. Many studies report short-term (3–12 months) results for blood pressure and arterial stiffness. The primary endpoints were changes in 24 h mean systolic blood pressure (BP) and office systolic BP 48 months after RDN. The secondary endpoints were changes in aortic pulse wave velocity and impact of polypharmacy on these variables. Materials and Methods: Renal artery denervation was performed in 73 patients treated for resistant hypertension; 49 patients remained in final analysis. Patient examination was carried out before the procedure, and subsequently at 3, 6, 12, 24, and 48 months later. Patients’ antihypertensive and overall medication regimens were carefully analysed. Results: Mean 24 h arterial blood pressure lowered and was sustained at lower levels for up to 48 months; median (interequartile range—IQR) from 158(23.5)/100(14.2) to 140(26.5)/86(16.2) mmHg. Mean reduction in 24 h ambulatory systolic BP was −11 ± 25 mmHg (95% CI, −20 to −2; p < 0.001), while office systolic BP reduced by −7 ± 23 mmHg (95%CI, −24 to −1; p < 0.02). A significant reduction in median aortic pulse wave velocity 12 months after the procedure (drop from baseline 11.2 [3.15] m/s (95%CI 6.1 to 16.2) to 9.8 [2.1] m/s (95%CI 6.1 to 13.7; p = 0.002)). After 48 months, there was no worsening compared to the baseline level of 10.3 [4.0] m/s (95% CI 6.9 to 17.8) (p > 0.05). The total mean number of antihypertensive drugs remained unchanged: 5.97(±1.1) vs. 5.24 (±1.45). A higher number of pills after 48 months was associated with higher aortic pulse wave velocity (1–5 pill group: 8.1 ± 1.6 m/s; 6–10 pill group: 10.9 ± 1.8 m/s; >11 pill group: 15.1 ± 2.6 m/s) (p = 0.003). Conclusions: Antihypertensive effect after renal denervation lasts up to 48 months with no worsening of arterial stiffness compared to baseline. In our study, polypharmacy was associated with increased arterial stiffness 48 months after the procedure.
BackgroundConsumer smartwatches have gained attention as mobile health (mHealth) tools able to detect atrial fibrillation (AF) using photoplethysmography (PPG) or a short strip of electrocardiogram (ECG). PPG has limited accuracy due to the movement artifacts, whereas ECG cannot be used continuously, is usually displayed as a single-lead signal and is limited in asymptomatic cases.ObjectiveDoubleCheck-AF is a validation study of a wrist-worn device dedicated to providing both continuous PPG-based rhythm monitoring and instant 6-lead ECG with no wires. We evaluated its ability to differentiate between AF and sinus rhythm (SR) with particular emphasis on the challenge of frequent premature beats.Methods and ResultsWe performed a prospective, non-randomized study of 344 participants including 121 patients in AF. To challenge the specificity of the device two control groups were selected: 95 patients in stable SR and 128 patients in SR with frequent premature ventricular or atrial contractions (PVCs/PACs). All ECG tracings were labeled by two independent diagnosis-blinded cardiologists as “AF,” “SR” or “Cannot be concluded.” In case of disagreement, a third cardiologist was consulted. A simultaneously recorded ECG of Holter monitor served as a reference. It revealed a high burden of ectopy in the corresponding control group: 6.2 PVCs/PACs per minute, bigeminy/trigeminy episodes in 24.2% (31/128) and runs of ≥3 beats in 9.4% (12/128) of patients. AF detection with PPG-based algorithm, ECG of the wearable and combination of both yielded sensitivity and specificity of 94.2 and 96.9%; 99.2 and 99.1%; 94.2 and 99.6%, respectively. All seven false-positive PPG-based cases were from the frequent PVCs/PACs group compared to none from the stable SR group (P < 0.001). In the majority of these cases (6/7) cardiologists were able to correct the diagnosis to SR with the help of the ECG of the device (P = 0.012).ConclusionsThis is the first wearable combining PPG-based AF detection algorithm for screening of AF together with an instant 6-lead ECG with no wires for manual rhythm confirmation. The system maintained high specificity despite a remarkable amount of frequent single or multiple premature contractions.
Introduction.Rapid eye movement (REM) sleep-related bradyarrhythmia syndrome is characterized by pathological asystoles during the REM sleep phase. It is a rare rhythm disorder, being reported only few times in the literature. Due to non-specific symptoms, REM sleep-related bradyarrhythmia might be often underdiagnosed. Other cardiac diseases associated with pathological sinus arrests must be excluded to establish the correct diagnosis of and appropriate therapy for REM sleep-related bradyarrhythmia. We report a case of this syndrome followed by hypertension and diastolic heart failure.The case.A 49-year-old male with severe hypertension presented for a cardiologist’s consultation. His main complaints were palpitations, fatigue, dyspnoea, and snoring. Polysomnography test revealed a normal sleep structure with episodes of bradycardia and increased parasympathetic activity during phasic events of REM sleep. Heart rate variability Poincare plot analysis demonstrated similar results. REM sleep-related bradyarrhythmia syndrome was diagnosed and patient was treated with dual chamber heart pacemaker implantation.Discussion.Various components of the autonomic nervous system influence the development of REM sleep-related bradyarrhythmia syndrome. The main factor is likely an increased vagal tone during the phasic REM sleep with the absence of normal compensatory sympathetic activity. Concomitant hypertension in REM sleep-related bradyarrhythmia syndrome is caused by a paradoxically abnormal control of the autonomic nervous system and can be explained through the acetylcholine metabolism pathway. Best suited diagnostic and treatment options for REM sleep-related bradyarrhythmia syndrome are discussed.Conclusions.Patients with REM sleep-related bradyarrhythmia syndrome often present with indistinct symptoms. Polysomnography is an essential diagnostic test for the differential diagnosis of various nocturnal arrhythmias and sleep disorders. Severe hypertension is a common complication of sleep disorders and requires appropriate treatment of the underlying condition. An implantation of a heart pacemaker is the first-choice treatment for patients with REM sleep-related bradyarrhythmia syndrome.
Aims Readmission and mortality are the most common and often combined endpoints in acute heart failure (AHF) trials, but an association between these two outcomes is poorly investigated. The aim of this study was to determine whether unplanned readmission is associated with a greater subsequent risk of death in patients with acute dyspnoea due to cardiac and non-cardiac causes. Methods and results Derivation cohort (1371 patients from the LEDA study) and validation cohort (1986 patients from the BASEL V study) included acute dyspnoea patients admitted to the emergency department. Cox regression analysis was used to determine the association of 6 month readmission and the risk of 1 year all-cause mortality in AHF and non-AHF patients and those readmitted due to cardiovascular and non-cardiovascular causes. In the derivation cohort, 666 (49%) of patients were readmitted at 6 months and 282 (21%) died within 1 year. Six month readmission was associated with an increased 1 year mortality risk in both the derivation cohort [adjusted hazard ratio (aHR) 3.0 (95% confidence interval, CI 2.2-4.0), P < 0.001] and the validation cohort (aHR 1.8, 95% CI 1.4-2.2, P < 0.001). The significant association was similarly observed in AHF (aHR 3.2, 95% CI 2.1-4.9, P < 0.001) and other causes of acute dyspnoea (aHR 2.9, 95% CI 1.9-4.5, P < 0.001), and it did not depend on the aetiology [aHR 2.2, 95% CI 1.6-3.1 for cardiovascular readmissions; aHR 4.1, 95% CI 2.9-5.7 for non-cardiovascular readmissions (P < 0.001 for both)] or timing of readmission. Conclusions Our study demonstrated a long-lasting detrimental association between readmission and death in AHF and non-AHF patients with acute dyspnoea. These patients should be considered 'vulnerable patients' that require personalized follow-up for an extended period.
High-sensitivity troponin assay brought new challenges as we detect elevated concentration in many other diseases, and it became difficult to distinguish the real cause of this elevation. In this notion, diagnosis of acute coronary syndrome (ACS) remains a challenge in emergency department (ED). We aim to examine different approaches for rule-in and rule-out of ACS using risk scores, copeptin, and coronary computed tomography angiography (CCTA). A prospective observational study was designed to evaluate chest pain patients. Consecutive adult patients admitted to the ED with a chief complaint of chest pain due to any cause were included. All patients were followed-up for 6 months after discharge for major adverse cardiovascular events and readmissions. Admission data, ED processes, and diagnoses were analyzed. One hundred forty-six patients were included, average age was 63 ± 13.4 years, and 95 (65.1%) were male. Global Registry of Acute Coronary Events (GRACE) and History, ECG, Age, Risk factors, Troponin (HEART) scores showed good prognostic abilities, but HEART combination with copeptin improves diagnoses of myocardial infarction (area under the curve [AUC] 0.764 vs AUC 0.864 P = .0008). Patients with elevated copeptin were older, had higher risk scores, and were more likely to be admitted to hospital and diagnosed with ACS in ED. For copeptin, AUC was 0.715 (95% confidence interval 0.629–0.803), and for combination with troponin, AUC of 0.770 (0.703–0.855) did not improve rule-in of myocardial infarction. High-sensitivity troponin I assay alongside prior stroke, history of carotid stenosis, dyslipidemia, use of diuretics, and electrocardiogram changes (left bundle branch block or ST depression) are good predictors of myocardial infarction (χ² = 52.29, AUC = 0.875 [0.813–0.937], P < .001). The regression analysis showed that combination of copeptin and CCTA without significant stenosis can be used for ACS rule-out (χ² = 26.36, P < .001, AUC = 0.772 [0.681–0.863], negative predictive value of 96.25%). For rule-in of ACS, practitioner should consider not only scores for risk stratification but carefully analyze medical history and nonspecific electrocardiogram changes and even with normal troponin results, we strongly suggest thorough evaluation in chest pain unit. For rule-out of ACS combination of copeptin and CCTA holds great potential.
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