SEARCH OF THE STRESS INDUSED VENTRICULAR TACHICARDIA REASONS — THE METABOLIC THERAPY OPPORTUNITIES

A clinical case of a 56-year-old man is presented in which only ventricular tachycardia without clinical and ECG criteria of myocardial ischemia is recorded on the exercise test. The ventricular tachycardia was the only reason for stopping the test. This clinical case demonstrates all the difficulties in determining the genesis of ventricular arrhythmias induced by exercise. The purpose of the work was to show all the difficulties in determining the genesis of exercise-induced ventricular arrhythmia. The literature references related to the exercise-induced ventricular arrhythmia differentiation is rather poor. It is only known that if a patient develops and progresses ventricular arrhythmia, a tredmill test is considered questionable. Exerciseinduced ventricular arrhythmias especially ventricular tachycardia, are the most dangerous. Therefore, additional diagnostic methods were used to reveal the main disease as the background of ventricular tachycardia. Results of pharmacological test with nitroglycerine were the indication of the ischemic origin of ventricular tachycardia. Coronary angiography did not reveal coronary artery stenoses. Positron emission tomography revealed coronary microcirculation disturbance after which a decision about metabolic therapy with Mexicor was made. The correct choice of the drug (Mеxisor) was confirmed by the results of control studies — improvement of metabolism and antiarrhythmic effect. The article concludes that the choice of the treatment exercise-induced ventricular arrhythmia in patients with stable coronary artery disease should be individual and pathogenetic.

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Significance of exercise-induced ventricular arrhythmia in stable coronary artery disease: A coronary artery surgery study project

The American Journal of Cardiology ◽

10.1016/s0002-9149(84)80064-8 ◽

1984 ◽

Vol 54 (10) ◽

pp. 1182-1188 ◽

Cited By ~ 60

Author(s):

Magdi Sami ◽

Bernard Chaitman ◽

Lloyd Fisher ◽

David Holmes ◽

David Fray ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Ventricular Arrhythmia ◽

Stable Coronary Artery Disease ◽

Coronary Artery Surgery ◽

Artery Disease ◽

Exercise Induced ◽

Coronary Artery Surgery Study

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Comorbid conditions - a reason to strengthen antianginai therapy in patients with stable coronary artery disease

Medical alphabet ◽

10.33667/2078-5631-2021-23-49-52 ◽

2021 ◽

pp. 49-52

Author(s):

O. L. Barbarash ◽

V. V. Kashtalap

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Stable Angina ◽

Clinical Case ◽

Stable Coronary Artery Disease ◽

Mechanisms Of Action ◽

Functional Class ◽

Second Line ◽

Comorbid Conditions ◽

Artery Disease

In the article on the example of a clinical case approaches to enhancing antianginal therapy of coronary artery disease were discussed. Arguments were given for prescribing preparations of the second line of antianginal agents (thymetazidine) in the patient with stable angina with high functional class and concomitant hypotonia after a complicated COVID-19. The main mechanisms of action of trimetazidine and results of clinical studies were discussed.

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Exercise induced ventricular arrhythmias Angiographic correlation with the severity of coronary artery disease.

Japanese Heart Journal ◽

10.1536/ihj.24.489 ◽

1983 ◽

Vol 24 (4) ◽

pp. 489-502 ◽

Cited By ~ 5

Author(s):

Lorenzo DECAPRIO ◽

Sergio CUOMO ◽

Carlo VIGORITO ◽

Anna GIUNTA ◽

Massimo ROMANO ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Ventricular Arrhythmias ◽

Artery Disease ◽

Exercise Induced

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P1603Nicorandil suppresses ischemia-induced cardiac interstitial norepinephrine enhancement and ventricular arrhythmia in hypertrophic hearts

European Heart Journal ◽

10.1093/eurheartj/ehz748.0362 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

M Kobara ◽

N Naseratun ◽

Y Watanabe ◽

H Toba ◽

T Nakata

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Ventricular Tachycardia ◽

Ventricular Arrhythmia ◽

Ventricular Arrhythmias ◽

Sham Group ◽

Cardiac Tissue ◽

Norepinephrine Release ◽

Norepinephrine Concentration ◽

Ischemic Period

Abstract Background Myocardial infarction (MI) is a major cause of death in western countries and Japan, and hypertension is a major risk factor of MI. In hypertensive heart, acute myocardial infarction often leads to lethal ventricular arrhythmia. Nicorandil, an ATP sensitive potassium channel (KATP) opener, is usually used in the treatment of acute myocardial infarction. The effects of nicorandil on ischemic myocyte are fully defined. On the other hand, KATP in neuroterminals is known to regulate norepinephrine release, but the effect of nicorandil on ischemic norepinephrine release in cardiac tissue has remained unexplored. Purpose We examined whether nicorandil suppressed norepinephrine release via neuronal KATP and ventricular arrhythmia during acute ischemia in pressure overload-induced hypertrophic hearts. Methods SD Rats were divided into two groups; abdominal aortic constriction (AAC) group and sham-operated (Sham) group. Four weeks after constriction, cardiac geometry and function were examined using echocardiography. Then, myocardial ischemia was induced by the left anterior descending artery occlusion for 100 minutes in the presence or absence of intravenous infusion of nicorandil. Cardiac interstitial norepinephrine concentration in ischemic region was measured using the microdialysis method and concentration of cyclic AMP, a second messenger of norepinephrine, in cardiac tissue was measured by ELISA. Ventricular arrhythmias were monitered by ECG during whole ischemic period. Results Four weeks after constriction, remarkable left ventricular wall thickening was observed in AAC group. Before ischemia, ventricular arrhythmia was not found in both groups. Number of ventricular arrhythmia, including ventricular tachycardia and ventricular fibrillation, was increased in early ischemic period (- 40 min) in both groups, and was grater in AAC group. Before ischemia, interstitial norepinephrine concentration in cardiac tissue was higher level in AAC group than in Sham group. Ischemia obviously increased norepinephrine concentration in both groups time dependently and AAC further increased norepinephrine than Sham group. Concentration of cyclic AMP in cardiac tissue was raised in early ischemic period (- 40 min) and then gradually decreased. Nicorandil significantly suppressed the number of ventricular arrhythmias, and abolished the ventricular tachycardia and fibrillation without hemodynamic alterations. Nicorandil also attenuated norepinephrine and cAMP enhancement in acute ischemic period in both groups. Conclusion Ischemia-induced ventricular arrhythmia was more frequent and severe in hypertrophic hearts and interstitial norepinephrine enhancement may play a role in this ischemic arrhythmia. Nicorandil suppressed ischemia-induced interstitial norepinephrine release by neuronal KATP opening, which attenuated ventricular arrhythmias in normal and hypertrophic hearts.

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