Morphological Re-Evaluation of Cardiac Sarcoidosis　― A Case-Based Analysis of 14 Post-Mortem Japanese Hearts ―

Abstract

Background: Cardiac sarcoidosis is a major cause of secondary cardiomyopathy leading to lethal arrhythmias and heart failure; however, identifying specific imaging findings of cardiac sarcoidosis remains a major issue. We re-examined the macroscopic morphology of post-mortem hearts to identify and reconfirm crucial findings for the clinical diagnosis of cardiac sarcoidosis.

Methods and Results: We examined 14 autopsied hearts from patients who were diagnosed with cardiac sarcoidosis from 2002 to 2019 at several medical institutions in Japan. The cases were classified into 2 groups: ante-mortem diagnosis (Group A, n=8), and post-mortem diagnosis (Group B, n=6). Of the 14 hearts, steroids were only administered in Group A. Seven macroscopic features were re-evaluated in all hearts: (1) epicardial irregularity (n=5); (2) fibrosis in the posterior interventricular junction (n=11); (3) ventricular septum wall thinning (n=9); (4) diffuse left ventricular wall thinning (n=4); (5) ventricular aneurysms (n=3); (6) papillary muscle deformities (n=12); and (7) white colored fibrosis (n=8).

Conclusions: This study highlights the underreported macroscopic findings of cardiac sarcoidosis. The 7 features highlight the uniqueness of cardiac sarcoidosis, which warrants recognition of this disease as a distinct pathological entity rather than merely a dilated cardiomyopathy-like secondary cardiomyopathy.

Cardiac sarcoidosis is a major cause of secondary cardiomyopathy, which can lead to lethal cardiac arrhythmia and congestive heart failure in advanced stages. Accurate diagnosis of cardiac sarcoidosis during the clinical course is essential for appropriate treatment and improved patient outcomes. Diagnosis of cardiac sarcoidosis is largely dependent on imaging techniques, such as echocardiography and cardiac magnetic resonance; however, identifying specific findings for cardiac sarcoidosis remains a major issue. Given these limitations, cardiologists require more information regarding the specific morphological findings of cardiac sarcoidosis.

Roberts et al.¹ provided a comprehensive report on the morphology of cardiac sarcoidosis, which detailed typical macroscopic patterns and characteristics. Matsui et al.² proposed macroscopic and histological patterns of fatal cardiac sarcoidosis based on a Japanese autopsy series. Sporadic cases from various medical backgrounds (e.g., medication, mechanical devices, and surgical therapy, such as cardiac transplantation) and subsequent reviews, including meta-analyses, have been reported.^3,4 However, autopsy case series in Japan remain limited,^5–7 and recognizing detailed lesion characteristics is crucial and requires further understanding to improve the diagnosis of cardiac sarcoidosis in clinical practice. Therefore, this study aimed to reanalyze the macroscopic pathology of post-mortem hearts to identify specific findings of sarcoidosis using autopsy examination.

Methods

Fourteen autopsied hearts that were diagnosed with cardiac sarcoidosis between 2002 and 2019 was re-examined macroscopically. Autopsy examinations were conducted at the following hospitals: Showa Medical University Hospital, Tokyo (n=4); Showa Medical University Fujigaoka Hospital, Yokohama (n=1); Yokufukai Hospital, Tokyo (n=1); Kawasaki Kyodo Hospital, Kawasaki (n=1); National Cerebral and Cardiovascular Center, Suita (n=5); Kochi University Hospital, and Chikamori Hospital, Nangoku, Kochi (n=2). Hearts were divided into 2 groups: diagnosed with cardiac sarcoidosis before death (Group A: ante-mortem diagnosis, n=8), or during autopsy examination (Group B: post-mortem diagnosis, n=6). This study conforms with the principles outlined in the Declaration of Helsinki, and was approved by the Showa Medical University Research Ethics Review Board (Reference no. 22-200-B).

Macroscopic photos of the hearts pathologically diagnosed with cardiac sarcoidosis at autopsy examination were re-examined, both before and after formalin fixation. The images included an overview of the whole epicardial surface, 4-chamber cross-sections, and transverse cross-sections of both ventricles. Seven macroscopic features were identified and analyzed in all hearts: (1) irregular, rough epicardial aspect; (2) fibrous lesion in the posterior interventricular junction; (3) ventricular septum wall thinning; (4) diffuse ventricular wall thinning with dilated cardiomyopathy-like cavity; (5) focal aneurysm of the left ventricular free wall; (6) papillary muscle deformity (atrophic change or fibrosis); and (7) white colored replacement fibrosis.

Results

The hearts were from 9 (64.3%) women and 5 (35.7%) men, and the mean age at the time of death was 68.8±12.6 years (range 45–99 years). The patient profiles and re-examined pathological findings in both groups are shown in Table. Age and gender trends were similar to a previous Japanese report.⁸ Three patients in Group A were confirmed to have cardiac sarcoidosis based on endomyocardial biopsy, and another 3 patients were diagnosed as systemic sarcoidosis by lymph node or skin biopsies. The other 2 patients (case no. 4, and case no. 8) in Group A were confirmed to have cardiac sarcoidosis based on ventricular septal wall thinning on echocardiography.

Table.

Patient Profiles and Pathologic Findings of the Hearts

	Age/sex	Clinical information					Pathological findings
		Fatal condition	Steroid	AV block	VT	Device implantation	Heart weight (g)	1	2	3	4	5	6	7
								Epicardial irregularity	Fibrosis in the posterior interventricular junction	Wall thinning of the ventricular septum	Diffuse left ventricular wall thinning	Ventricular aneurysm (free wall)	Papillary muscle deformity	White colored fibrosis
Group A
No. 1	59/F	HF	+	−	+	CRT-D	700	N/A	+	N/A	±	−	+	+
No. 2	63/M	LA	+	−	+	ICD	520	+	+	−	−	+	+	+
No. 3	64/M	HF	+	−	+	CRT-D	505	+	+	+	−	+	+	−
No. 4	65/F	HF	+	−	+	CRT-D	495	−	N/A	+	+	+	+	−
No. 5	65/F	SD	+	+	−	PM	610	−	+	+	−	−	+	−
No. 6	66/F	SD	+	+	+	PM	677	+	−	+	−	−	+	+
No. 7	67/M	HF	+	+	+	ICD	490	+	+	+	±	−	+	+
No. 8	86/F	HF	+	−	−	−	498	−	+	+	−	−	+	−
	Mean 66.9		n=8 (100%)	n=3 (37.5%)	n=6 (75%)		Mean 562	n=4 (50%)	n=6 (75%)	n=6 (75%)	n=1 (7.1%)	n=3 (37.5%)	n=8 (100%)	n=4 (50%)
Group B
No. 9	45/F	SD	−	+	−	PM	705	−	+	−	−	−	+	+
No. 10	63/M	HF	−	+	−	PM	270	+	+	+	+	−	+	+
No. 11	64/F	HF	−	−	+	CRT-D	610	N/A	+	±	+	−	+	−
No. 12	76/F	HF	−	+	N/A	PM	540	−	+	+	−	−	−	+
No. 13	81/M	HF	−	−	−	CRT-D	350	−	−	+	+	−	−	−
No. 14	99/F	HF	−	−	−	CRT-D	380	−	+	−	−	−	+	+
	Mean 71.3		n=0 (0%)	n=3 (50%)	n=1 (16.7%)		Mean 476	n=1 (16.7%)	n=5 (83.3%)	n=3 (50%)	n=3 (50%)	n=0 (0%)	n=4 (66.7%)	n=4 (66.7%)
Total	Mean 68.8		n=8 (57.1%)	n=6 (42.9%)	n=7 (50%)		Mean 525	n=5 (35.7%)	n=11 (78.6%)	n=9 (64.3%)	n=4 (28.6%)	n=3 (21.4%)	n=12 (85.7%)	n=8 (57.1%)

AV, atrioventricular; CRT-D, cardiac resynchronization therapy-defibrillator; F, female; HF, heart failure; ICD, implantable cardioverter defibrillator; LA, lethal arrhythmia (VT/VF); M, male; N/A, not available (no photo information); PM, pacemaker; SD, sudden death; VF, ventricular fibrillation; VT, ventricular tachycardia.

Clinical Information

The major causes of death were heart failure (n=10) and sudden cardiac death or lethal arrhythmia (n=4). Steroids were administered to all patients in Group A. Three cases of atrioventricular block were observed in each group. Ventricular tachycardia was observed in 6 patients in Group A and in 1 patient in Group B before death. Pacemaker devices, including defibrillators, were implanted in 13 (92.9%) cases.

Pathological Findings

Irregular, Rough Epicardial Aspect The hearts exhibited unexpected shape variations (Figure 1). The mean heart weight was >500 g, but some cases showed no significant increase (<400 g; range 270–705 g). Five hearts (Group A, n=4; Group B, n=1) showed an irregular epicardial surface, suggesting epicardial shrinkage caused by post-inflammatory replacement fibrosis. Four (50%) cases in Group A may have been influenced by steroid administration. The shrinking lesions deformed the overall shape of the heart, shortening the longitudinal length. This may concern with the different mechanisms for fibrosis during granulomatous inflammatory change in active cardiac sarcoidosis and the post-fibrotic change (attenuation) of matured burned-out fibrous lesions due to steroid administration.

Figure 1.

Representative epicardial anterior view of cardiac sarcoidosis. (A) Overall enlargement of the heart similar to dilated cardiomyopathy phenotype (case no. 12, 76-year-old woman). The epicardial surface was preserved, smooth, and homogeneous (bar=1 cm). (B) The epicardial surface has an irregular appearance, small dimples, and shrinkage (yellow arrows; case no. 3, 64-year-old man). (C) The heart was less dilated and the weight did not increase (270 g; case no. 10, 63-year-old man). The epicardial surface has a rough appearance.

Fibrous Lesion in the Posterior Interventricular Junction Fibrotic lesions were observed in 11 (78.6%) hearts on the epicardial side of the posterior wall at the right and left interventricular junctions in the transverse slices of both ventricles (Figure 2). This area is one of the most common sites for cardiac sarcoidosis and can be the initial lesion that leads to septal thinning and aneurysmal formation.

Figure 2.

Representative fibrotic lesions in the transverse cross-section of both ventricles. (A) Simple isolated whitish fibrotic lesion at the epicardial side of the posterior right and left ventricular junction (yellow arrow; case no. 12, 76-year-old woman). The left ventricular cavity is slightly dilated without significant wall thinning (bar=1 cm). (B) White colored irregular fibrosis lesions in varying sizes are distributed in both ventricles, including the area of the posterior right and left ventricular junction (case no. 9, 45-year-old woman). The left ventricular cavity is dilated and less wall thinning is observed. (C) White fibrotic lesion located in the posterior right and left ventricular junction. Left ventricular wall thickening is observed without thinning of the posterolateral wall (yellow arrow; case no. 2, 63-year-old man).

Ventricular Septum Wall Thinning Ventricular septum wall thinning is a typical abnormality in cardiac sarcoidosis. Thinning of the upper portion was observed in 9 (69.2%) of 13 hearts (Group A, n=6; Group B, n=3; 1 heart was not available for observation; Figure 3A). One heart (case no. 3) showed thinning of the ventricular septum (Figure 3B), while 3 (23.1%) hearts showed no significant ventricular septum wall thinning (Figure 3C).

Figure 3.

Representative longitudinal section of the right and left atriums and ventricles (4-chamber view). (A) The summit of the ventricular septum is regionally thinned with fibrosis. The thinned wall curves to the right ventricle, which is affected by blood flow pressure (yellow arrow; case no. 8, 86-year-old woman; posterior-anterior side view). The anterior wall of the atrioventricular junction beneath the mitral valve is consecutively thinned, extending from the thinned septal lesion. (B) The ventricular septal wall is completely thinned from the atrioventricular junction to the apex edge (case no. 3, 64-year-old man; anterior-posterior side view). Thinned lesions extend to both ventricles. Black colored lesions indicate radiofrequency ablation sites for eliminating ventricular tachycardia. (C) The thickness of the ventricular septal wall is well preserved (case no. 2, 63-year-old man). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Diffuse Left Ventricular Wall Thinning as a Phenotype of Dilated Cardiomyopathy Wall thinning was observed in the left ventricular wall, resembling the appearance of dilated cardiomyopathy in the short axis of both ventricles. Among the 14 hearts, 4 (28.6%; Group A, n=1; Group B, n=3) showed a dilated cavity with diffuse thinning of the ventricular free wall (dilated cardiomyopathy-like phenotype). The thinned left ventricular wall was not transmurally replaced by post-inflammatory fibrosis.

Focal Aneurysm of the Left Ventricular Free Wall Small localized ventricular aneurysms were observed in 3 hearts in Group A, all located in the lateral wall near the basal area beneath the mitral valve annulus (Figure 4). The longitudinal dimensions (basal to apex side) were 22, 27, and 35 mm in cases 2, 3, and 4, respectively. The thinned aneurysmal wall did not bulge towards the epicardium, and endocardial trabeculation was preserved and relatively prominent.

Figure 4.

Representative images of localized left ventricular free wall aneurysm. (A) The left ventricular wall is thinned regionally (27 mm in longitudinal length). The fibrotic lesion is prominent in the epicardial side and shows an irregular aspect (yellow arrow). The endocardial trabecula is relatively preserved and shows a complicated endocardial surface in the aneurysm (case no. 3, 64-year-old man; posterior-anterior side view). (B) The left ventricular wall is focally thinned without aneurysmal bulge towards the epicardial side (yellow arrow; 22 mm in length; case no. 2, 63-year-old man). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Papillary Muscle Deformity (Atrophic Change or Fibrosis) Shortening, deformity, and fibrotic atrophy were observed in 12 (85.7%) hearts, leading to tendinous cord stretching and a tethering effect for mitral regurgitation (Figure 5). One heart (case no. 2) had a radiofrequency-ablated lesion (black spot) at the papillary muscle base for ventricular tachycardia therapy.

Figure 5.

Representative lesions of the papillary muscle. (A) Fibrotic atrophy of the papillary muscle. The base of the papillary muscle shows continuous fibrosis and shows an irregular epicardial aspect (yellow arrows; case no. 7, 67-year-old man). (B) The papillary muscle is deformed and shortened (case no. 3, 64-year-old man). The tendinous cords are stretched by the lesion. Black colored lesions indicate radiofrequency ablation sites for eliminating ventricular tachycardia. LA, left atrium; LV, left ventricle.

White-Colored Replacement Fibrosis Two patterns of fibrotic lesions were observed in half of the hearts: a distinct white colored replacement fibrosis with relatively less ventricular wall thinning (Figure 2) and a semi-transparent fibrosis with wall thinning. White colored fibrosis was observed in 4 hearts without steroid administration (66.7%; Group B) and 5 hearts with steroid administration (50%; Group A).

Discussion

Sarcoidosis is a systematic inflammatory disease, and cardiac involvement is characterized by inflammatory cell infiltration and post-inflammatory fibrosis. The distribution patterns of granulomatous inflammatory lesions are distinct and differ from those of other inflammatory cardiac diseases, such as in acute myocarditis or organization after ischemic necrosis. Post-inflammatory fibrosis also shows a distinct pattern from other cardiomyopathies or ischemic fibrosis,⁹ sometimes even presenting with a normal appearance.¹⁰

Advanced imaging modalities, such as echocardiography, gadolinium-enhanced magnetic resonance, and fluorodeoxyglucose positron emission tomography, have been used for diagnosing cardiac sarcoidosis in clinical settings and are recommended in the guidelines of the Japanese Society of Cardiology.¹¹ However, the limitations of these imaging modalities have not been thoroughly resolved, and a number of cases remain undiagnosed before death.^12,13 These suggest that some morphological findings in cardiac sarcoidosis can be indefinite or misunderstood. In this study, we identified macroscopic, previously underreported, characteristics and compared them with the clinical information in our Japanese case series.

Epicardial Irregularity (Rough Epicardial Surface)

Fibrotic lesions in cardiac sarcoidosis predominantly spread on the epicardial side of the ventricular wall.¹ Fibrosis at the epicardial surface causes shrinkage and results in a rough and irregular epicardial aspect. This characteristic may contribute to overall shape deformity of the heart, particularly shortening in the longitudinal direction (Figure 1B,C). However, capturing these changes on the surface of the epicardium using current imaging modalities may be challenging.

Fibrous Lesions in the Posterior Interventricular Junction Between the Right and Left Ventricular Wall

The exact mechanism underlying fibrotic lesions in this region remains uncertain. The posterior interventricular junction is a crucial site of typical and initial cardiac sarcoidosis lesions,¹⁴ and positively enhanced lesions in this area can be detected using magnetic resonance imaging.¹⁵ The anterior side of the interventricular junction is also a common site of fibrosis. In cardiac magnetic resonance imaging, late gadolinium enhancement is often observed around the anterior and posterior basal septa in non-ischemic cardiomyopathy.¹⁶ The localization of fibrotic lesions is a key finding that suggests cardiac sarcoidosis or other cardiomyopathies.

Ventricular Septum Wall Thinning

Lesions in the ventricular septum are a well-known characteristic of cardiac sarcoidosis, which is frequently detected using echocardiography or cardiac magnetic resonance imaging.¹¹ These lesions usually originate from the ventricular junction (case no. 8), specifically in the upper part of the ventricular septum, which arises in the early phase of cardiac sarcoidosis. Due to the high systemic blood pressure from the left ventricle, the thinned septal region often curves toward the right ventricle and may develop a twisted deformity.¹ The ventricular septum is a frequent site for granulomatous lesions. The most significant wall thinning was observed in case no. 3, which showed entire thinning of the ventricular septum. In some cases (e.g., case no. 9), wall thinning was less pronounced despite the fibrotic lesions at the septum. The degree of wall thinning might be related to the duration of the inflammation and the progressive fibrosis associated with steroid administration.^1,17

Diffuse Left Ventricular Wall Thinning as a Phenotype of Dilated Cardiomyopathy

The major phenotype of cardiac sarcoidosis is dilated cardiomyopathy due to reduced ventricular contractions.¹⁴ Ventricular fibrosis in primary idiopathic dilated cardiomyopathy presents as a diffuse interstitial pattern that directly causes diffuse and significant left ventricular hypokinesis. However, only 3 cases in Group B showed a dilated cardiomyopathy phenotype in our case series. In contrast, cardiac sarcoidosis is primarily characterized by spotty granulomatous lesions with areas replaced by fibrotic lesions. As a result, the residual area of myocardial tissue that is free from the granulomatous lesion is histologically preserved, and the ventricular wall, which has less granulomatous and fibrotic lesions, are relatively thickened (Figures 2C,3B,C). Previous studies have also reported cases of ventricular wall thickening, with some cases being classified as hypertrophic cardiomyopathy.^18,19

Focal Aneurysm of the Left Ventricular Free Wall

Ventricular aneurysms are a specific finding in cardiac sarcoidosis.¹ Although ventricular aneurysms are relatively common after the late stages of myocardial infarction, those found in cardiac sarcoidosis have distinct characteristics. First, the aneurysms are small (approximately 2–3 cm), and the bulge to the epicardial side is not prominent in post-mortem hearts without contraction. However, in a living heart with active contraction, the shape would be more aneurysmal due to partial dyskinesis. Second, the location observed in our study was unique. They were often found near the basal side of the left ventricle, independent of coronary artery territories. Third, endocardial trabeculation is visible with a limestone-like appearance and less atrophic change. This suggests that wall thinning primarily occurred on the epicardial side and did not extend to the endocardial surface, which is typically found in ischemic changes. The location of the aneurysm near the basal site of the ventricular free wall is related to septal wall thinning and the interventricular junction, which are primary sites of sarcoid lesions. Therefore, a 3-dimensional assessment of the distribution of sarcoid lesions is required. Furthermore, the 3 cases observed with ventricular aneurysms were receiving steroid therapy, which may have contributed to aneurysm formulation by promoting advanced fibrosis.¹

Papillary Muscle Deformity (Atrophic Change or Fibrosis)

Lesions in the papillary muscle are another characteristic finding in cardiac sarcoidosis.¹ In the present study, more than 80% of the hearts had lesions in the papillary muscle. Atrophic changes due to extensive fibrosis and atrophic deformity with a shortened papillary muscle were prominent. These lesions resulted to stretching of the tendinous cords, which can cause a tethering effect for mitral regurgitation. Two hearts in the study had a history of mitral valve plasty. The reason why the papillary muscle is a frequent site for granulomatous lesions is uncertain; however, this structure is a crucial portion of the Purkinje fiber distribution that extends from the bundle branches, and has been described as an arrhythmogenic substrate that can cause lethal tachyarrhythmia.²⁰ One of the hearts in the study (case no. 3; Figure 5B) had undergone radiofrequency ablation therapy to eliminate lethal ventricular tachyarrhythmia.

White-Colored Replacement Fibrosis

The morphology of granulomatous fibrotic lesions is different from that of fibrosis in remote myocardial infarction. Fibrotic clusters were irregular in size, and their color was whitish in many cases (Figures 2,5A). The whitish color exhibits a semi-translucent impression and may have differences in the extracellular matrix of other diseases with fibrosis.^1,21 In contrast, non-whitish fibrotic lesions with atrophy and wall thinning may be related to the effects of steroid administration.¹⁷

Study Limitations

This study had some limitations. Cardiac sarcoidosis is a relatively rare disease, and opportunities for autopsy examination are limited. The present cases were enrolled from several medical institutions; however, the sample size remained small. The morphology of the hearts varied, which prevented statistical analyses. Further studies addressing these limitations is necessary to confirm our findings.

Conclusions

The morphological findings of the cardiac sarcoidosis cases were variable, with some unrecognized or underreported features. Considering the 7 factors identified, the unique morphological characteristics of cardiac sarcoidosis become evident. This reinforces the consideration that cardiac sarcoidosis should be considered as a distinct pathological entity rather than merely a dilated cardiomyopathy-like secondary cardiomyopathy.

Sources of Funding

None.

Disclosures

The authors declare that there are no conflicts of interest.

IRB Information

The study was approved by Showa Medical University Research Ethics Review Board (Reference no. 22-200-B).

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