Accessory papillary muscles and papillary muscle hypertrophy are associated with sudden cardiac arrest of unknown cause☆
Introduction
The major known causes of sudden cardiac arrest (SCA) are coronary artery disease, cardiomyopathies, and channelopathies [1]. During the last five decades, researchers have identified some causes of SCA that had been considered idiopathic SCA or idiopathic ventricular fibrillation. These include long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, Brugada syndrome, short QT syndrome, and early repolarization syndrome [2], [3], [4], [5], [6], [7]. However, the causes of SCA remain unknown in a considerable number of patients. Some forensic pathologists have reported autopsy cases of patients with sudden cardiac death who had accessory or anomalous papillary muscles (PMs) [8], [9]. Although the PMs are known to be an arrhythmogenic structure [10], it is not known whether they have any association with SCA. The present study was performed to elucidate the association between the morphology of the PMs of the left ventricle (LV) and SCA.
Section snippets
Study population and patient workup
The study design was approved by the institutional review board and was conducted in compliance with the Declaration of Helsinki. Informed consent and a critical event committee were exempted by the board because this was a retrospective study. We retrospectively evaluated 213 patients who were hospitalized because of out-of-hospital SCA in a single university hospital between January 2012 and October 2013. Among 213 patients, we included 190 patients who had undergone electrocardiography (ECG)
Baseline characteristics
Of the initial 213 patients screened, 23 were excluded because no imaging studies had been performed, leaving 190 patients with out-of-hospital SCA who had undergone at least one of cardiac imaging studies, including echocardiography or cardiac CT and MRI. The baseline characteristics of the unknown-cause group (n = 49; age 49.9 ± 15.9 years; 38 men) and in the known-cause group (n = 141; age 54.2 ± 16.6 years; 121 men) are given in Table 1. The patients in the unknown-cause group had a significantly
Discussion
The main finding of the present study was that the prevalence of accessory PM and PM hypertrophy was significantly higher in patients with SCA of unknown cause than in patients with SCA of known cause or in those without SCA. Furthermore, patients with accessory PMs or PM hypertrophy had a significantly greater risk of SCA of unknown cause.
The PMs of the LV begin to contract shortly before the ventricular systole and maintain tension in the chordae tendineae and mitral leaflets throughout
Study limitations
This was a retrospective study, in which the prevalence of accessory PMs and PM hypertrophy was evaluated in patients with SCA. It is not clear whether the associations between the accessory PMs or PM hypertrophy and SCA were causal; nor is it clear what role the accessory PMs and PM hypertrophy played in the development of SCA. There could be a selection bias because we excluded the patients who were not resuscitated from SCA and who could not undergo imaging study. We classified the patients
Conclusions
Accessory PMs and PM hypertrophy are associated with SCA of unknown cause. Further investigation is needed to clarify this association and to determine the mechanisms involved.
Grant support
This work was not supported by any funding.
Conflicts of interest
None.
Acknowledgments
The authors thank Mi Kyung Song, MS, and Bo Kyung Ma, MS, from Biostatistics Collaboration Unit, Yonsei University College of Medicine, for their statistical analyses.
References (41)
- et al.
The long Q–T syndrome
Am. Heart J.
(1975) - et al.
Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report
J. Am. Coll. Cardiol.
(1992) - et al.
Clinical characteristics and long-term prognosis of patients with variant angina. A comparative study between Western and Japanese populations
Int. J. Cardiol.
(1988) Left ventricular false tendons: anatomic, echocardiographic, and pathophysiologic insights
J. Am. Soc. Echocardiogr.
(2013)- et al.
Refinement of echocardiographic criteria for left ventricular noncompaction
Int. J. Cardiol.
(2013) - et al.
Anatomical and molecular mapping of the left and right ventricular His-Purkinje conduction networks
J. Mol. Cell. Cardiol.
(2011) - et al.
Catheter ablation of ventricular fibrillation: importance of left ventricular outflow tract and papillary muscle triggers
Heart Rhythm.
(2014) - et al.
Latent left ventricular outflow tract obstruction induced by abnormal hypertrophic papillary muscle caused myocardial ischemia
Int. J. Cardiol.
(2009) - et al.
Electrocardiographic characteristics of patients with false tendon: possible association of false tendon with J waves
Heart
(2012) Sudden cardiac death: exploring the limits of our knowledge
J. Cardiovasc. Electrophysiol.
(2001)
Bidirectional tachycardia in a child. A study using His bundle electrography
Br. Heart J.
Idiopathic short QT interval: a new clinical syndrome?
Cardiology
Sudden cardiac arrest associated with early repolarization
N. Engl. J. Med.
Augmentation of J waves and electrical storms in patients with early repolarization
N. Engl. J. Med.
Sudden cardiac death due to an anomalous posterior papillary muscle
Am. J. Forensic Med. Pathol.
Anomalous anterior papillary muscle as an autopsy finding in two cases
J. Forensic Sci.
Role of papillary muscle in the generation and maintenance of reentry during ventricular tachycardia and fibrillation in isolated swine right ventricle
Circulation
Frequency of provoked coronary spasms in patients undergoing coronary arteriography using a spasm provocation test via intracoronary administration of ergonovine
Angiology
Solitary papillary muscle hypertrophy as a possible form of hypertrophic cardiomyopathy
Jpn. Circ. J.
Distribution of the Purkinje fibres in the sheep heart
Anat. Rec.
Cited by (7)
The Role of the Submitral Apparatus in Hypertrophic Obstructive Cardiomyopathy
2023, Journal of the American Society of EchocardiographyCitation Excerpt :For a midventricular obstruction resulting from PM hypertrophy, additional resection is performed around the bases of the PMs. PMs that originate separately from the anterolateral and posteromedial PMs, or that branch into two or three bellies at the base of anterolateral and posteromedial PMs, are defined as accessory PMs28 (Figure 2). Accessory PMs may tether the MV to the LVOT, thus contributing to LVOTO.15
Possible association of papillary muscle hypertrophy with the genesis of J-waves
2020, Journal of CardiologyCitation Excerpt :The parasternal short-axis view at the level of the PMs at end-diastole was used for PM measurements. PM hypertrophy was considered to be present when at least one of the two (anterolateral and posteromedial) PMs had a diameter of ≥11 mm in a minor axis (Fig. 2) [5]. We confirmed the presence of PM hypertrophy after considering the other parasternal and apical echocardiographic views.
Morphology of hypertrophied basal septum contributes to left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy: a retrospective case-control study
2023, Quantitative Imaging in Medicine and SurgeryAnomalous papillary muscle insertion into mitral valve leaflet: Autopsy study and implications
2023, Journal of Forensic SciencesPapillary muscles. Dark side of the heart: A simple approach for a forgotten structure
2020, Echocardiography
- ☆
These authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.