Introduction: For patients with uncontrolled blood pressure (BP), differentiation of pharmacological resistance from inadequate or improper medication use is key to clinical management. A digital health feedback device (DHFD) has been developed, utilizing an Ingestible Sensor (IS) and Wearable Sensor (WS) to passively record medication taking and timing, and measure physiological and behavioral metrics such as heart rate, step count, activity and rest patterns. This study evaluated DHFD use in diagnosing the cause of persistent BP elevation. Methods: Patients with a history of BP (≥140/90) on ≥2 anti-hypertensives (AHs) at 6 primary care centers in the United Kingdom were prescribed the DHFD for 14 days. Patients co-ingested the IS along with their prescribed BP medications while continuously wearing the WS. BP was assessed on days 1 and 14. Results: A total of 151 patients were enrolled; 38% were taking ≥3 AHs at baseline; 144 patients (95%) completed the 2 planned weeks of DHFD use. Root cause of treatment unresponsiveness was identified by DHFD in 100% of completers; 58% had pharmacological resistance, and 42% had inadequate AH use. During DHFD use, mean systolic BP decreased significantly by -10±17 (p<0.001) and mean diastolic BP decreased significantly by -5±9 mmHg (p<0.001); 38% of subjects achieved BP control on their current therapy. Subsequent management included: medicines reviews and/or adherence counselling with no AH changes in 81%, medication changes in 13%, referrals to specialists in 1%, and no additional actions were taken in 6%. Majority of practices (75%) found the DHFD added value, and 83% of patients expressed a positive experience. Side effects were minimal, consisting of mainly minor skin irritation (8%), or gastrointestinal symptoms (3%). Two patients withdrew due to possibly-related adverse events. Conclusions: In subjects using the DHFD for uncontrolled BP while prescribed AHs, all received a more informed therapeutic intervention from their providers following DHFD use. BP control was achieved in 38% within 2 weeks. DHFD can facilitate evidence-based progression through the BP treatment pathway by differentiating which patients can achieve treatment goals with prescribed therapy from those who may require AH changes.
Blood coagulation studies were undertaken in patients of high altitude pulmonary oedema at 3,700 m, comparable controls, and sea level subjects to determine the possible causal connection between changes in fibrinolytic activity, blood coagulation factors, and formation of thrombi within the alveolar capillaries, venules and some branches of pulmonary arteries. The following changes have been observed: Fibrinolytic activity was reduced. Plasma fibrinogen and factor VIII were increased. Factor XII was decreased. Platelet adhesiveness and platelet factor 3 were increased and electrophoretic mobility of platelets reduced. The integrity of platelet plasma membrane, capacity of pseudopodia formation, and ability of degranulation remained intact. Both arterial and venous adenosine-5′-diphosphate (ADP) levels were low and there was evidence of excessive utilisation of ADP in the pulmonary bed. The findings suggest that sludging of RBCs and formation of thrombi possibly result from these changes, impede the pulmonary blood flow, and aggravate the disease.Apart from inducing diuresis and reducing pulmonary blood volume, within 30 minutes of its administration intravenously, furosemide enhances fibrinolytic activity, decreases factors V, VIII and X and thrombotest activity, increases factor XII, reduces platelet factor 3 and adhesiveness, and improves clot retraction. It seems imoediments to blood flow at capillary and venuiar level, which occur on account or the hypercoagulable state, are removed and pulmonary oedema is relieved.
Blood coagulation studies were carried out in 38 Indian soldiers who were resident at altitudes between 3690 and 5540 m for 2 years. Compared with 16 sea-level controls, 6 of these 38 subjects who had developed pulmonary hypertension during their stay at high altitude showed a significant increase of plasma fibrinogen, fibrinolytic activity, platelet adhesiveness, platelet factor 3, factor V, and factor VIII. In the remaining 32 subjects who did not develop pulmonary hypertension there was a significant increase of plasma fibrinogen and fibrinolytic activity only.The above differences between subjects who develop pulmonary hypertension at high altitude and those who do not develop pulmonary hypertension suggest that high altitude pulmonary hypertension is of occlusive origin and is dependent on changes in blood coagulation at high altitude.
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