scholarly journals Coronary endothelial dysfunction in the hypertensive patient: from myocardial ischemia to heart failure

1997 ◽  
Vol 11 (1) ◽  
pp. 45-49 ◽  
Author(s):  
JC Burnett
Keyword(s):  
Heart Failure ◽  
Endothelial Dysfunction ◽  
Myocardial Ischemia ◽  
Hypertensive Patient ◽  
Coronary Endothelial Dysfunction

Increased inactivation of nitric oxide is involved in coronary endothelial dysfunction in heart failure

2001 ◽  
Vol 280 (1) ◽  
pp. H68-H75 ◽  
Author(s):  
Kenichi Arimura ◽  
Kensuke Egashira ◽  
Ryo Nakamura ◽  
Tomomi Ide ◽  
Hiroyuki Tsutsui ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Endothelial Dysfunction ◽  
Lipid Peroxides ◽  
Canine Model ◽  
Oxygen Free Radical ◽  
Antioxidant Treatment ◽  
Synthesis Inhibitor ◽  
Intracoronary Infusion ◽  
Coronary Endothelial Dysfunction

Recent evidence suggests the possibility that enhanced inactivation of endothelium-derived nitric oxide (NO) by oxygen free radical (OFR) may cause endothelial dysfunction in heart failure (HF). To test this hypothesis, we examined the effect of antioxidant therapy on endothelium-dependent vasodilation of the coronary circulation in a canine model of tachycardia-induced HF. Endothelium-dependent vasodilation was less than that in controls, and OFR formation in coronary arterial and myocardial tissues was greater in HF dogs than those in controls. The immunohistochemical staining of 4-hydroxy-2-nonenal, OFR-induced lipid peroxides was detected in coronary microvessels of HF dogs. Intracoronary infusion of the cell-permeable OFR scavenger Tiron inhibited OFR formation and improved endothelium-dependent vasodilation in HF dogs but not in controls. The NO synthesis inhibitor N G-monomethyl-l-arginine (l-NMMA) diminished the beneficial effect of Tiron in HF dogs. Endothelium-independent vasodilation was similar between control and HF dogs, and no change in its response was noted by Tiron or Tiron plus l-NMMA in either group. In summary, antioxidant treatment with Tiron improved coronary vascular endothelium-dependent vasodilation by increasing NO activity in tachycardia-induced HF. Thus coronary endothelial dysfunction in HF may be, at least in part, due to increased inactivation of NO by OFR.

scholarly journals Coronary endothelial dysfunction occurs early in the pathophysiology of heart failure

2002 ◽  
Vol 39 ◽  
pp. 148-149
Author(s):  
Abhiram Prasad ◽  
Jassim Al Suwaidl ◽  
Stuart T. Higano ◽  
Geralyn M. Pumper ◽  
David R. Holmes ◽  
...  
Keyword(s):  
Heart Failure ◽  
Endothelial Dysfunction ◽  
Coronary Endothelial Dysfunction

Coronary Endothelial Dysfunction Precedes Heart Failure and Reduction of Coronary Reserve in Awake Dogs

1997 ◽  
Vol 29 (1) ◽  
pp. 217-227 ◽  
Author(s):  
Mathias Knecht ◽  
Daniel Burkhoff ◽  
Geng-Hua Yi ◽  
Sulli Popilskis ◽  
Shunichi Homma ◽  
...  
Keyword(s):  
Heart Failure ◽  
Endothelial Dysfunction ◽  
Coronary Reserve ◽  
Coronary Endothelial Dysfunction

scholarly journals The effect of ivabradine as part of standard therapy on vascular endothelial function and cardiac electrical instability in patients with post-infarction cardiosclerosis and heart failure

2020 ◽  
Vol 25 (1) ◽  
pp. 52-58
Author(s):  
A. A. Abdullaev ◽  
S. N. Mammaev ◽  
A. A. Anatova ◽  
U. A. Islamova ◽  
A. M. Makhacheva
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Endothelial Dysfunction ◽  
Myocardial Ischemia ◽  
Endothelial Function ◽  
Standard Therapy ◽  
Electrical Instability ◽  
Group 2 ◽  
Group 1

Aim. To reveal the equivalence of nebivolol replacement with ivabradine in the prevention of endothelial dysfunction and cardiac electrical instability in patients with heart failure with reduced ejection fraction (HFrEF).Material and methods. In current observational study, 126 patients with HFrEF in the postinfarction period were randomized into two groups for six-month treatment: group 1 (n=62) — standard therapy (acetylsalicylic acid 0,1 g/day, clopidogrel 75 mg/day, veroshpiron 50 mg/day, nebivolol 5 mg/day, perindopril 5 mg/day and rosuvastatin 20 mg/day; group 2 (n=66) — the same therapy with nebivolol replacement with ivabradine 10 mg/day. Initially and after 6 months, 24-hour Holter monitoring was performed, heart rate variability was determined. We also investigated endothelial dysfunction using the photoplethysmographic technique with post-occlusive reactive hyperemia (PORH) test.Results. The heart rate, the number of episodes and the duration of symptomatic and silent myocardial ischemia, total myocardial ischemia were significantly decreased in both groups (p<0,001). The decrease of supraventricular extrasystole frequency in both groups had not statistical significance (p>0,05). In both groups, after therapy, parameters of heart rate variability were improved with the parasympathetic predominance (p<0,01). In both groups, the PORH test revealed the increase of brachial artery diameter (group 1 — 5,90Ѓ}3,15% and group 2 — 5,88Ѓ}1,82%) and pulse wave amplitude (group 1 — 1,81Ѓ}0,78 and group 2 — 1,73Ѓ}0,90 times), which indicates a trend towards an improvement in endothelial function. Intergroup comparisons did not reveal significant differences.Conclusion. Ivabradine is equivalent to nebivolol in preventing ventricular extrasystole and reducing heart rate, number of episodes of symptomatic and silent ischemia and the duration of total myocardial ischemia in patients with HFrEF. Ivabradine equivalently to nebivolol improves endothelial function and heart rate variability with reducing the sympathetic activity.

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