Effect of Direct Oral Anticoagulants for Ulcer Epithelization and Laser Doppler Flowmetry Parameters In Patients with Diabetic Foot Syndrome and Atrial Fibrillation

Aim. To study changes in epithelialization of diabetic foot ulcers and parameters of laser Doppler flowmetry (LDF) in patients with diabetic foot syndrome (DFS) and atrial fibrillation (AF) during complex therapy with the addition of direct oral anticoagulants (DOAC).Material and methods. An open-label comparative randomized study in parallel groups was performed. Patients with neuroischemic DFS and persistent FA without previous anticoagulant therapy were randomized into two groups: combination therapy for DFS and rivaroxaban (group 1; n=24) or combination therapy for DFS and dabigatran (group 2; n=22). Changes in local status in diabetic foot ulcers, coagulogram parameters and LDF were studied at 4 and 12 weeks.Results. Complete epithelialization of diabetic foot ulcers after 12 weeks was found in 14 (58.3%) patients in group 1, and in 10 (45.4%) patients in group 2. Statistically significant improvements in LDF parameters were found in both groups in both groups: an increase in the microcirculation index by 53.5% (p=0.02), pulse wave by 124.0% (p=0.003), respiratory wave by 59.4% (p=0.007) was found in group 1. An increase in the microcirculation index by 48.5% (p=0.02), pulse wave by 73.1% (p=0.003), respiratory wave by 47.1% (p=0.03) were found in group 2.Conclusion. Positive statistically significant changes in epithelialization of diabetic foot ulcers and LDF parameters were found in patients with DFS and AF during 12 weeks of complex therapy with the addition of DOACs (rivaroxaban and dabigatran). Further research for DOACs in DFS patients is needed.

Abstract 17184: An Increase in the Respiratory Effort Immediately Intensifies the Hemodynamic Congestion; a Mechanism for Progressive Cardiac Decompensation

Introduction: An increase in the pulmonary wedge pressure (PCWP) is associated with an increase in the respiratory effort and the sensation of dyspnea. Hypothesis: We investigated the inverse cause and effect relationship, whether an increase in the respiratory effort can by itself aggravate the hemodynamic congestion. Methods: We scrutinized the cardiopulmonary interactions by simultaneously measuring hemodynamic and respiratory indices in heart failure (HF) patients undergoing right heart catheterization. The immediate effects of the respiratory effort on the hemodynamic indices were analyzed by asking the patients to perform short events of apnea and intentional vigorous breathing. The cardiac waves are superimposed on the respiratory waves in the PCWP. To quantify the respiratory effort, the PCWP was decomposed into cardiac and respiratory waves. The respiratory effort (PRESP) was defined as the peak to peak swing in the respiratory wave that modulated the PCWP. Results: HF patients (n=38) exhibited a high PRESP of 9.0±3.2 mmHg, ~3.5-fold higher than the reported normal respiratory effort. The end-expiratory PCWP rose with PRESP, by 0.83±0.06 mmHg for every 1 mmHg of PRESP (p<0.01). The pulmonary artery pressure (PAP) rose with PRESP by 1.40±0.09 mmHg for every 1 mmHg of PRESP. The changes in the respiratory effort had immediate effect on PCWP, within a single breathing-cycle (t =1.67±0.40 s) in all patients. Interestingly, similar changes in the PCWP with PRESP were obtained in all the patients, independently of the HF etiology. Conclusions: An increase in the respiratory effort is not just a result of cardiac decompensation. The respiratory effort has immediate detrimental effects on the PCWP, PAP and the workloads of the heart. The results highlight the existence of a cardiopulmonary vicious cycle the can lead to progressive decompensation, where the respiratory effort plays a pivotal role.

Deriving respiration from pulse wave: a new signal-processing technique

Investigations of autonomic nervous system activity using spectral analysis of heart rate (HR) and blood pressure (BP) variability is very popular in many scientific disciplines, and yet only half of all studies involving spectral analysis control for respiration. Because respiration modulates HR and BP variability, knowledge of the respiratory rate is necessary for the proper interpretation of HR and BP power spectra. We devised and validated a new signal-processing technique to derive respiration from the blood pressure wave. This technique is based on the relationship between oscillations in the area under the dicrotic notch of the pulse wave and respiration. The results of our view signal-processing technique yielded significant correlations between protocols of the actual number of respiratory cycles and our blood pressure-derived respiratory cycles and their respective spectra for a number of standard autonomic tests (P < 0.05). Our method will allow retrospective extraction of the respiratory wave and as such afford a more precise interpretation of HR and BP spectra.

Effect of lung inflation on lung blood volume and pulmonary venous flow

Phasic changes in lung blood volume (LBV) during the respiratory cycle may play an important role in the genesis of the respiratory wave in arterial pressure, or pulsus paradoxus. To better understand the effects of lung inflation on LBV, we studied the effect of changes in transpulmonary pressure (delta Ptp) on pulmonary venous flow (Qv) in eight isolated canine lungs with constant inflow. Inflation when the zone 2 condition was predominant resulted in transient decreases in Qv associated with increases in LBV. In contrast, inflation when the zone 3 condition was predominant resulted in transient increases in Qv associated with decreases in LBV. These findings are consistent with a model of the pulmonary vasculature that consists of alveolar and extra-alveolar vessels. Blood may be expelled from alveolar vessels but is retained in extra-alveolar vessels with each inflation. The net effect on LBV and thus on Qv is dependent on the zone conditions that predominate during inflation, with alveolar or extra-alveolar effects being greater when the zone 3 or zone 2 conditions predominate, respectively. Lung inflation may therefore result in either transiently augmented or diminished Qv. Phasic changes in left ventricular preload may therefore depend on the zone conditions of the lungs during the respiratory cycle. This may be an important modulator of respiratory variations in cardiac output and blood pressure.