<p>The first description of sudden cardiac death was made by Hippocrates in the 4th century BC [<span>1</span>]. Such cases of sudden collapse and death have intrigued both the public and medical science for centuries and a practical definition is that sudden cardiac death is the unexpected and natural death from a cardiac cause within a short period, usually less than 1 h from the onset of symptoms, in a person without any known prior condition [<span>1, 2</span>]. Sudden cardiac death (SCD) is clearly the end-result of a wide variety of cardiac conditions—both congenital and acquired. However, the most common mechanism for the event of SCD is ventricular fibrillation [<span>1</span>].</p><p>Understandably, SCD can afflict both the athlete and the non-athlete and is the cause of 13%–20% of all deaths in Western countries [<span>2</span>]. In athletes older than 35 years of age atherosclerotic coronary artery disease is the most common cause of SCD, while primary cardiomyopathies and ion channelopathies are more commonly found in the young athlete with SCD [<span>2</span>]. However, this is an evolving field of study and the recent study published by Stojanovic et al. [<span>3</span>] is of great importance as it links two well-known risk factors for SCD—left ventricular hypertrophy (LVH) and QT-dispersion [<span>4</span>]. The strong association between LVH and overall cardiovascular mortality first emerged from the Framingham heart study [<span>4</span>]. Initially, after this observation, several studies have confirmed the strong association between LVH and cardiovascular mortality, but the specific association with sudden cardiac death (SCD) came later with the Oregon Sudden Unexpected Death Study (Oregon SUDS)–one of the first to confirm the link between LVH and SCD [<span>4, 5</span>]. The development of LVH creates various pathways to ventricular arrhythmogenesis, which include ventricular ectopy, in fact, every additional millimeter of left ventricular wall thickness increases the risk of ventricular ectopy 2- to 3-fold [<span>4</span>]. LVH is the cause of significant cellular and interstitial remodeling of the myocardium which promotes ventricular arrhythmogenesis from both re-entry and triggered activity [<span>4</span>]. An increase in left ventricular mass (LVH) results in various myocardial alterations resulting in electrical remodeling with resultant prolonged QRS intervals, prolonged OT intervals, interstitial fibrosis with re-entry, sub-endocardial ischemia and increased sensitivity to pro-arrhythmia due to an increase in left ventricular wall stress [<span>4</span>]. In fact, all forms of left ventricular hypertrophy, concentric, eccentric, and even concentric remodeling without hypertrophy are all associated with an increased risk for sudden cardiac death [<span>6</span>].</p><p>The QT interval—the interval from the beginning of the QRS complex to the end of the T wave on the surface ECG—represents the period of global ventricu
{"title":"The Evolving Science on Sudden Cardiac Death—The Marriage of Left Ventricular Hypertrophy and QT-Dispersion","authors":"James Ker","doi":"10.1111/echo.70026","DOIUrl":"10.1111/echo.70026","url":null,"abstract":"<p>The first description of sudden cardiac death was made by Hippocrates in the 4th century BC [<span>1</span>]. Such cases of sudden collapse and death have intrigued both the public and medical science for centuries and a practical definition is that sudden cardiac death is the unexpected and natural death from a cardiac cause within a short period, usually less than 1 h from the onset of symptoms, in a person without any known prior condition [<span>1, 2</span>]. Sudden cardiac death (SCD) is clearly the end-result of a wide variety of cardiac conditions—both congenital and acquired. However, the most common mechanism for the event of SCD is ventricular fibrillation [<span>1</span>].</p><p>Understandably, SCD can afflict both the athlete and the non-athlete and is the cause of 13%–20% of all deaths in Western countries [<span>2</span>]. In athletes older than 35 years of age atherosclerotic coronary artery disease is the most common cause of SCD, while primary cardiomyopathies and ion channelopathies are more commonly found in the young athlete with SCD [<span>2</span>]. However, this is an evolving field of study and the recent study published by Stojanovic et al. [<span>3</span>] is of great importance as it links two well-known risk factors for SCD—left ventricular hypertrophy (LVH) and QT-dispersion [<span>4</span>]. The strong association between LVH and overall cardiovascular mortality first emerged from the Framingham heart study [<span>4</span>]. Initially, after this observation, several studies have confirmed the strong association between LVH and cardiovascular mortality, but the specific association with sudden cardiac death (SCD) came later with the Oregon Sudden Unexpected Death Study (Oregon SUDS)–one of the first to confirm the link between LVH and SCD [<span>4, 5</span>]. The development of LVH creates various pathways to ventricular arrhythmogenesis, which include ventricular ectopy, in fact, every additional millimeter of left ventricular wall thickness increases the risk of ventricular ectopy 2- to 3-fold [<span>4</span>]. LVH is the cause of significant cellular and interstitial remodeling of the myocardium which promotes ventricular arrhythmogenesis from both re-entry and triggered activity [<span>4</span>]. An increase in left ventricular mass (LVH) results in various myocardial alterations resulting in electrical remodeling with resultant prolonged QRS intervals, prolonged OT intervals, interstitial fibrosis with re-entry, sub-endocardial ischemia and increased sensitivity to pro-arrhythmia due to an increase in left ventricular wall stress [<span>4</span>]. In fact, all forms of left ventricular hypertrophy, concentric, eccentric, and even concentric remodeling without hypertrophy are all associated with an increased risk for sudden cardiac death [<span>6</span>].</p><p>The QT interval—the interval from the beginning of the QRS complex to the end of the T wave on the surface ECG—represents the period of global ventricu","PeriodicalId":50558,"journal":{"name":"Echocardiography-A Journal of Cardiovascular Ultrasound and Allied Techniques","volume":"41 11","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/echo.70026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142570193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Toshimitsu Tsugu, Kaoru Tanaka, Yuji Nagatomo, Mayuko Tsugu, Johan De Mey
L/P ratio, which indicates the proportion of lumen volume to plaque volume of the vessel, is lower in lesion than in per-lesion (RCA, 0.9 vs. 7.7; LAD, 1.4 vs. 8.1; and LCX, 0.9 vs. 8.0). For lesion located in the middle segments of the three major vessels, FFRCT drops from 0.97 to 0.78 for RCA, from 0.94 to 0.55 for LAD, and from 0.99 to 0.72 for LCX, respectively. Invasive coronary angiography shows moderate stenosis in the middle segment of the RCA but no significant obstructive coronary disease at the sites where FFRCT showed a substantial decline in the LAD and LCX. CCTA indicates coronary CT angiography; ICA, invasive coronary angiography; LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right coronary artery; SOCAD, significant obstructive coronary disease.