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Amiloride HCl Dihydrate in coronary artery disease: improving erythrocyte potassium-oxigen binding and reversion of angina and ST-T alterations.

Session Poster session 1

Speaker Carlos Delgado

Event : ESC Congress 2017

  • Topic : coronary artery disease, acute coronary syndromes, acute cardiac care
  • Sub-topic : Coronary Artery Disease (Chronic)
  • Session type : Poster Session

Authors : C Delgado (Valencia,VE), A Delgado-Almeida (Valencia,VE), MC Delgado-Lelievre (Miami,US)

C. Delgado1 , A. Delgado-Almeida1 , M.C. Delgado-Lelievre2 , 1University of Carabobo and Venezuelan Foundation of HF, Unidad de Investigaciones Clínicas, Instituto Docente de Nefrologia y Urologia - Valencia - Venezuela , 2Cardiovascular Disease Prevention Wellness Research - Miami - United States of America ,

European Heart Journal ( 2017 ) 38 ( Supplement ), 195

Background: Following our discovery that red-blood-cell potassium (RBC-K) was involved in K-O2 binding by deoxyhemoglobin, we explored the hypothesis that increasing RBC-K would improve K-O2 binding and O2Sat% in cardiovascular diseases.

Objective: To confirm our findings that increasing blood O2Sat% by Amiloride HCl Dihydrate (AHD) reverses angina and ECG alterations in single-blind trial of CHD (NCT01231165).

Methods: A randomized double-blind trial, placebo-controlled clinical trial of AHD (2-years) was conducted in 100 patients (female with angina, ST-T alterations and inherited defect of low RBC-K, despite optimal medical therapy for angina and atherosclerosis. Serial ECG, non-invasive central aortic BP and hemodynamic, ion transport research studies and echocardiograms were performed. Statistical analysis performed with SAS System, p<0.05 considered significant.

Results: Compared with placebo, the AHD rapidly improved RBC-K content, angina (87% of cases, 1.4±0.3 weeks, CI: 1.51 to 1.29), CCS Class (1.6±0.7 vs 3.1±0.8, p<0.001), vs (3.2±0.6 vs 3.3±0.4, p=0.21), and Duke Treadmill Score (7.9±4.2 vs -4.75±4.4 p=0.0001) and exercise time (7.9±2.8, CI: 9.36 to 6.44) vs (5.3±2.5 min, CI: 6.77 to 3.83, p<0.05). Reversion of angina was sustained through the next 6-months (87% vs 35% placebo, RR2.1, odds ratio 6.31, Pearson χ2 34.6, p<0.0001 at 95% CI) and 1-year (87% vs 29% placebo). After 6-months of AHD, ECG became normal (35% vs 0%, RR ∞ uncalculated-time, odds ratio ∞, Pearson χ2 42.4 at 95% CI, p<0.0001), improved (50% vs 24%; RR2.1, odds ratio 3.16, 95% CI, p<0.0001) or unchanged (15% vs 76%). At 1-year, 15 patients (27%) on AHD exhibited evidence of electrical regeneration of the heart, not observed with placebo. With these results, the 2nd year trial was an open label AHD trial in all 100 patients: 54 cases in the AHD group were free of angina, 85% from the previous placebo group. Venous blood from control subjects exposed to AHD (25 μg) rapidly increased O2Sat% (87±3% vs 47±6%, p<0.0001) and RBC-K binding (87±2.3 vs basal 93.0±2.3 mmol/lc, p<0.0001).

Conclusion: AHD improves K-O2 binding and O2Sat%, reversing angina and ST-T alterations in all CHD patients: 54 during the two years trial, and 46 in the Placebo group during the 2nd year open-label trial of AHD, including patients with new R-voltages in older and recent infarctions (NCT01228214).

Electrical Regeneration in Old Infarcts

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