Low Serum Levels of Eicosapentaenoic Acid and Docosahexaenoic Acid are Risk Factors for Cardiogenic Syncope in Patients with Brugada Syndrome

Yagi, Shusuke; Soeki, Takeshi; Aihara, Ken‐ichi; Fukuda, Daiju; Ise, Takayuki; Kadota, Muneyuki; Bando, Shigenobu; Matsuura, Tomomi; Tobiume, Takeshi; Yamaguchi, Koji; Kusunose, Kenya; Yamada, Hirotsugu; Wakatsuki, Tetsuzo; Shimabukuro, Michio; Akiyama, Masashi; Sata, Masataka

doi:10.1536/ihj.16-278

Cited by 11 publications

(9 citation statements)

References 27 publications

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“…We reported that low serum EPA and DHA levels are risk factors for cardiogenic syncope in patients with Brugada syndrome 75 ) . Although the etiology of Brugada syndrome is multifactorial and involves genetic, environmental, and hormonal components, n-3 PUFAs can modulate cardiac ion channels, resulting in the prevention of ventricular arrhythmia.…”

Section: Other Preferable Effects Of N-3 Pufas For Preventing Cvdmentioning

confidence: 97%

n-3 Polyunsaturated Fatty Acids: Promising Nutrients for Preventing Cardiovascular Disease

Yagi

Fukuda

Aihara

et al. 2017

J Atheroscler Thromb

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The adoption of the Western-style diet, with decreased fish intake and lack of exercise, has increased the prevalence of cardiovascular disease (CVD) in Japan. Statin treatment has been established to reduce the risk of cardiovascular events; however, 60%–70% of these events occur despite its use. Thus, the residual risk for CVD should be identified and resolved to reduce further cardiovascular events. The serum levels of n-3 polyunsaturated fatty acids (PUFAs), including eicosapentaenoic acid and docosahexaenoic acid, are reportedly associated with an increased incidence of cardiovascular events and mortality, whereas the addition of n-3 PUFA treatment to the statin treatment decreases cardiovascular events. Similar to statins, n-3 PUFAs have pleiotropic effects in addition to lipid-modifying effects. Pre-clinical and clinical studies have shown that n-3 PUFAs prevent cardiovascular events by ameliorating endothelial function and attenuating lipid accumulation, vascular inflammation, and macrophage recruitment, thereby causing coronary plaque development and rupture. Taken together, n-3 PUFAs are comprehensively able to attenuate the atherogenic response. Therefore, n-3 PUFA intake is recommended to prevent cardiovascular events, particularly in patients with multiple cardiovascular risk factors.

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Section: Other Preferable Effects Of N-3 Pufas For Preventing Cvdmentioning

confidence: 97%

n-3 Polyunsaturated Fatty Acids: Promising Nutrients for Preventing Cardiovascular Disease

Yagi

Fukuda

Aihara

et al. 2017

J Atheroscler Thromb

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“…38) Previous reports have described the secondary prevention of sudden cardiac death and ventricular arrhythmias after myocardial infarction or heart failure via the use of omega-3 PUFAs. 39) The cardioprotective effects of ω-3 PUFAs are thought to be due to synergism among multiple mechanisms. 36) The results of previous studies and those of the present study suggest that the improvement of coronary microcirculation by EPA may protect against microvascular ischemia or reperfusion injury when AMI occurs in patients with stable AP.…”

Section: Discussionmentioning

confidence: 99%

Lower Circulating Omega-3 Polyunsaturated Fatty Acids Are Associated with Coronary Microvascular Dysfunction Evaluated by Hyperemic Microvascular Resistance in Patients with Stable Coronary Artery Disease

et al. 2018

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The consumption of omega-3 polyunsaturated fatty acids (PUFAs) reduces the incidence of cardiovascular events and sudden cardiac death. Coronary microvascular dysfunction (CMD) is a predictor of cardiac mortality, but little information is known on the relationship between CMD and omega-3 PUFAs. This study aimed to identify the relationship between the serum levels of omega-3 PUFAs and the CMD evaluated by the hyperemic microvascular resistance index (hMVRI) to assess coronary microvascular function in patients with stable coronary artery disease (CAD). Intracoronary physiological variables (fractional flow reserve (FFR), hMVRI, mean distal coronary pressure (Pd), and average peak velocity (APV)) were measured in 108 patients. These parameters were evaluated in 150 coronary arteries with stenosis of intermediate severity and without significant ischemia (FFR > 0.80). The PUFA levels and atherosclerotic risk factors were also measured. Univariate analysis shows that hMVRI was negatively correlated with eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio (β = −0.31, P = 0.001) and EPA (β = −0.25, P = 0.009) and was positively correlated with dihomo-γ-linolenic acid (β = 0.26, P = 0.006). Multivariate regression analysis shows that the EPA/AA ratio was the only independent determinant of hMVRI (β = −0.234, SE = 0.231, P = 0.024). Furthermore, hMVRI decreased significantly from the lowest to highest tertiles of the EPA/AA ratio (P = 0.007). The EPA/AA ratio was positively correlated with APV at hyperemia (β = 0.26, P = 0.008) but not with Pd at hyperemia. A lower serum EPA/AA ratio may cause CMD in patients with stable CAD.

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“…For example, acute application of polyunsaturated fatty acids, in particular those of the n-3 class (PUFAs), inhibits I Na ( 97 ) and therefore may facilitate BrS. Yagi et al ( 98 ), however, suggested that n-3 PUFAs may prevent ventricular fibrillation in BrS, likely due to additional blockade of various other cardiac ion channels ( 68 ), including I to ( 99 ). High cholesterol and fat intake may constitute additional diet-related modulatory factors.…”

Section: Variable Expressivity In Scn5a Channelopamentioning

confidence: 99%

Disease Modifiers of Inherited SCN5A Channelopathy

Verkerk

Amin

Remme

2018

Front. Cardiovasc. Med.

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To date, a large number of mutations in SCN5A, the gene encoding the pore-forming α-subunit of the primary cardiac Na+ channel (NaV1.5), have been found in patients presenting with a wide range of ECG abnormalities and cardiac syndromes. Although these mutations all affect the same NaV1.5 channel, the associated cardiac syndromes each display distinct phenotypical and biophysical characteristics. Variable disease expressivity has also been reported, where one particular mutation in SCN5A may lead to either one particular symptom, a range of various clinical signs, or no symptoms at all, even within one single family. Additionally, disease severity may vary considerably between patients carrying the same mutation. The exact reasons are unknown, but evidence is increasing that various cardiac and non-cardiac conditions can influence the expressivity and severity of inherited SCN5A channelopathies. In this review, we provide a summary of identified disease entities caused by SCN5A mutations, and give an overview of co-morbidities and other (non)-genetic factors which may modify SCN5A channelopathies. A comprehensive knowledge of these modulatory factors is not only essential for a complete understanding of the diverse clinical phenotypes associated with SCN5A mutations, but also for successful development of effective risk stratification and (alternative) treatment paradigms.

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Low Serum Levels of Eicosapentaenoic Acid and Docosahexaenoic Acid are Risk Factors for Cardiogenic Syncope in Patients with Brugada Syndrome

Cited by 11 publications

References 27 publications

n-3 Polyunsaturated Fatty Acids: Promising Nutrients for Preventing Cardiovascular Disease

n-3 Polyunsaturated Fatty Acids: Promising Nutrients for Preventing Cardiovascular Disease

Lower Circulating Omega-3 Polyunsaturated Fatty Acids Are Associated with Coronary Microvascular Dysfunction Evaluated by Hyperemic Microvascular Resistance in Patients with Stable Coronary Artery Disease

Disease Modifiers of Inherited SCN5A Channelopathy

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