The variability of pressure in the cutaneous lymph capillaries on the forefoot was determined in 2 groups of healthy volunteers. In group A, including 12 subjects (8 men, 4 women; mean age 28 years, range 22 to 37 years) measurements were performed in the morning and late afternoon of the same day. In group B (12 subjects, 5 women, 7 men; mean age 53 years, range 23 to 72 years) measurements of lymph capillary pressure were repeated within an interval of 7 weeks. The superficial microlymphatics were visualized by intravital fluorescence microlymphography, cannulated with glass micropipettes, and the lymph capillary pressure was measured using a servo-nulling pressure system. The lymph capillary pressure measured in the morning (mean 7.54.4 mm Hg; range 4 to 16 mm Hg) did not differ (pb0.05) from the pressure in the late afternoon (mean value 5.63.4 mm Hg; range 1 to 13 mm Hg). In group B initial lymph capillary pressure (mean 3.92.9 mm Hg, range 1.1 to 9.7 mm Hg) was not different (pb0.05) compared to the pressure after 7 weeks (2.92.7 mm Hg; range 1.0 to 6.8 mm Hg). In conclusion, lymph capillary pressure in healthy subjects does not exhibit significant changes during the daytime and the long-term reproducibility is good.
Funding Acknowledgements Kantonsspital Olten, Switzerland Background In patients with chronic hepatitis C virus (HCV) infection, a higher risk for pulmonary artery hypertension (PAH) has been described after interferon (IFN) therapy. With the development of direct-acting antiviral (DAA) agents, vast improvements have been made in tolerance and less complications of HCV treatment. However, except of a few case reports, to date no clinical study about the evidence of PAH in patients with DAA medication for HCV infection has been published. We hypothesized that in patients, who receive DAA medication for HCV-infection, the systolic pulmonary artery pressure (sPAP) will not change significantly during and after competition of the therapy and there may be a lower post treatment risk for PAH within the population. Methods We prospectively enrolled patients who underwent treatment with DAA for chronic HCV infection. The patients received a transthoracic echocardiography (TTE) for the measurement of the pulmonary artery pressure before, during (8 weeks after starting the medication) and 8 weeks after completion of the HCV medication for evaluation of sPAP (figure 1). The whole treatment period took 8-12 weeks. Results Between June 2016 and October 2018, 33 patients completed the study protocol. In mean, the patient’s age was 50.1 ± 1.4 years and 30% of the population were female. Three patients (9 %) were HCV and human immunodeficiency virus (HIV) coinfected. The patients received different treatment regimens, according to hepatitis C genotype and co-medication. The left ventricular systolic and diastolic function were normal in all patients before treatment was started (left ventricular ejection fraction 60.7% [59.7 – 61.7%], E/A 1.18 [1.0 – 1.37]). The following table depicts the right ventricular parameter before the DAA therapy was started, 8 weeks after therapy start, and 8 weeks after therapy was completed. The analysis showed no significant difference between the sPAP in all three groups (25.9 ± 1.2 mmHg vs. 26.0 ± 1.3 mmHg vs.26.9 ± 1.1 mmHg, p-value 0.37, see figure). Conclusion DAA-therapy in chronic HCV infected patients is not associated with PAH in a follow-up of 2 months after the treatment was completed. Echocardiography Data Echocardiography data Before DAA medication was started 8 weeks after DAA-therapy 8 weeks after completion of DAA-therapy p-Value Right ventricular fractional area change (FAC), % 49.1 ± 1.4 51.7 ± 1.0 51.8 ± 1.1 0.09 Tricuspid Annular Plane Systolic Excursion (TAPSE), mm 25.2 ± 1.1 25.8 ± 0.7 24.3 ± 0.5 0.4 Right ventricular/right atrial gradient, mmHg 19.9 ± 1.0 20.5 ± 0.9 21.0 ± 0.8 0.24 Systolic pulmonary artery pressure (sPAP), mmHg 25.9 ± 1.2 26.0 ± 1.3 26.9 ± 1.1 0.37 Abstract P834 Figure. Multiple variable graph of sPAP
No abstract
Dilated cardiomyopathy is the most common form of cardiomyopathy and the second leading cause of left ventricular dysfunction with highly variable clinical presentation and prognosis. The clinical courses vary and are strongly heterogeneous, ranging from asymptomatic patients to those suffering from intractable heart failure or sudden cardiac death due to arrhythmias. Previous studies have reported a 10 years cardiovascular mortality up to 40% in developed countries, due to advanced heart failure or sudden cardiac death. However, the prognosis of dilated cardiomyopathy patients is variable and depends on multiple risk factors. This chapter provides a review of dilated cardiomyopathy with specific focus on the pathophysiological aspects and genetic etiology of the disease.
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