eISSN: 2084-9869
ISSN: 1233-9687
Polish Journal of Pathology
Current issue Archive Manuscripts accepted About the journal Supplements Editorial board Abstracting and indexing Subscription Contact Instructions for authors Ethical standards and procedures
SCImago Journal & Country Rank
vol. 72
Original paper

Wax hearts: seeking the antiquity of cardiac pathology

Rosa Henriques de Gouveia
Raffaella Santi
Roberta Ballestriero
Francesco M. Galassi
Lina Carvalho
Gabriella Nesi

University of Coimbra, Portugal
Careggi Teaching Hospital, Florence, Italy
University of the Arts, London, United Kingdom
Flinders University, Australia
University of Florence, Italy
Pol J Pathol 2021; 73 (4): 346-352
Online publish date: 2022/03/08
Article file
- 07-PJP-02242.pdf  [3.85 MB]
Get citation
JabRef, Mendeley
Papers, Reference Manager, RefWorks, Zotero


Wax, from the old English wºx, weax, of Germanic origin [1], consists of a long-chain fatty acid linked through an ester oxygen to a long-chain alcohol. It is insoluble in water but soluble in organic, non-polar solvents. Natural waxes, such as beeswax and the wax coating on the outer surface of the plant cuticle, are generally mixtures and melt more readily than the pure components [2].
Wax modelling is a procedure that has been used since the dawn of ancient civilizations. Wax could be easily modelled by hand or melted and cast employing the moulage technique [3, 4, 5, 6]. By the end of the 17th century, through the joint work of the Sicilian wax sculptor Gaetano Giulio Zumbo (1656-1701) and the French surgeon Guillaume Desnoues (1650-1735), the first models for medical teaching had been produced. Subsequently, until the beginning of the 20th century, wax models held a prominent position as teaching tools for medical students and professionals [3, 4, 5, 6]. Due to the complex configuration of the heart, three-dimensional (3D) models are of the utmost importance to understand both the morphological and pathophysiological features of this organ [7].
Herein, we present a joint study carried out on the 19th century heart wax models held in two antique and internationally renowned Pathology Museums at the Universities of Florence, Italy, and Coimbra, Portugal. This work aims to draw attention to the cultural treasure epitomised by unique cardio-pathological collections from a historical perspective, potentially catalysing a renovated interest in these models as ancillary didactic devices in medical education.

Material and methods

The Pathology Museum of the University of Florence, established in 1824, is currently housed at Careggi University Hospital, and among its specimens are eight heart wax models (Fig. 1). The Pathology Museum of the University of Coimbra, founded in 1822, is now located at the Anatomical and Molecular Pathology Institute of Coimbra’s Faculty of Medicine, and holds ten heart wax models (Fig. 2). All models were morphologically examined and photographed. The morphological lesions were then contextualized according to current medical practice.


A comprehensive inventory of the cardiac waxes from both collections is provided in Tables I and II. Scrutiny yielded a total of 18 cases, of which 5 were congenital cardiopathies, 3 metabolic disorders or degeneration of the heart, 5 infectious diseases of the heart or their complications (Fig. 3A, B), 2 degenerative valve diseases, and 3 hypertrophic or dilated heart conditions (Fig. 4).


In the 19th century, medical diagnosis was essentially clinical, lacking state-of-the-art imaging facilities, and therapeutic options were indeed limited. At this time, Florence and Coimbra Universities had high-quality medical schools, which adopted teaching tools such as anatomical and pathological wax models, admired throughout Europe. It was mainly for educational purposes that scientific ceroplastics was developed in the 18th and 19th centuries [6, 8, 9].
A pliable, widely accessible material, wax allowed the creation of realistic and durable models. Until the advent of colour photography, there existed no other medium capable of accurately reproducing diseases, and recording improvement or deterioration of patient conditions.
The Florentine heart wax models were created by Egisto Tortori (1829-1893) and Giuseppe Ricci, while the heart wax models in Coimbra were acquired from the Vasseur-Tramond workshop in Paris. They were accomplished either by direct observation of the diseased heart at autopsy in Florence, or by reproduction of a former wax model in Coimbra [4, 5].
Egisto Tortori, pupil of Luigi Calamai (1800-1851), was the last wax modeller from the La Specola workshop, where he started as an apprentice at the age of fifteen. Between 1771 and 1893 collections of both normal and diseased body parts were produced for the La Specola Museum and also for Italian and foreign universities. Tortori’s hearts are among the last vestiges of a long tradition of scientific ceroplastics, which flourished in Florence and subsequently spread across Europe. In the mid-19th century, other countries replaced Italy as the major producers of anatomical wax models [4, 5].
The Vasseur-Tramond workshop was founded in Paris by Pierre Vasseur, who was joined by his son-in-law Gustave Tramond (1846-1905) in 1878. As in Florence, artists collaborated closely with anatomists in order to make accurate models that, according to Gustave Tramond, “are not useful for studying anatomy but rather for remembering it once it has been learnt” [4, 5].
The types of cardiac disease and the presence of similar wax models in both series testify to the relevance of these disorders at that time. Indeed, congenital malformations, dilation, infections and their consequences were major causes of morbidity and mortality. Are these wax models still of any use?
Congenital heart malformations were a leading cause of death, particularly during the neonatal period and early infancy [10, 11, 12]. Nowadays, survival has greatly increased due to echocardiography and surgical/haemodynamic procedures [13]. However, adequate visualization of the malformed heart helps to easily recognize the defect and decide on the best corrective approach. Therefore the use of wax models during medical training is undoubtedly advantageous. Interventricular communication (ventricular septal defect = IVC = VSD) is the most frequent congenital cardiopathy (25-64%) [14, 15]. Survival into adulthood and old age may cause further complications, such as endocarditis, paradoxical embolization, cardiac insufficiency, arrhythmias and sudden death [13, 16, 17, 18, 19]. Univentricular heart, defined as a heart with “only one chamber fulfilling the criteria of a ventricle (the main chamber), with or without a coexisting rudimentary outlet chamber or trabecular pouch”, has a poor prognosis [20]. Over the years, the concept of purely morphological malformations has changed to that of functionally univentricular hearts, as has palliative surgery to more definitive corrective procedures [20, 21, 22].
Myocardial hypertrophy (eccentric, concentric, bilateral, right or left) was first described by the French physician Jean-Baptiste de Sènac (1693-1770) [23]. It may be primary or secondary to altered conditions of haemodynamic overload. Gross and microscopic characterization is therefore mandatory in order to establish the causal diagnosis, provide appropriate care and offer familial counselling in genetic-based diseases, such as hypertrophic cardiomyopathy (HCM) [24, 25, 26, 27, 28]. Exercise-induced hypertrophy is currently a crucial issue and investigation is imperative to avoid sudden cardiac death in sportspersons [29, 28, 30].
Sedentarism and change in dietary habits are two of today’s social/health “cancers”, since they have aggravated and/or introduced a variety of pathological disorders, namely obesity cardiomyopathy [31]. Emphasis has been laid upon the role of visceral fat as a cause of morbidity and in the development/vulnerability of coronary artery plaques [32]. Due to either genetic predisposing factors such as familial hypercholesterolaemia (then unknown) or excessive food consumption, epicardial fat deposition (cardiac adiposity, Quain fatty heart) has been observed and recorded [33, 34].
Endocarditis was another common cause of death, primarily because the principles and rituals of antisepsis both in and out of medical settings were in the early stages of development and mass antibiotic treatment with penicillin was not introduced until 1945 [35, 36, 37, 38]. All the valves could be involved (mitral valve > 25%), at times associated with systemic and/or local complications, such as leaflet rupture/perforation, cord and/or papillary muscle rupture and septic embolism [39, 40]. Endocarditis may be caused by several bacterial or fungal agents [41, 42, 43, 44]. Rheumatic valvular disease was once the usual underlying lesion, but nowadays this has been supplanted by degenerative processes, e.g. aortic valve calcification and mucoid degeneration of the mitral valve. Endocarditis can be isolated or associated with myocarditis, leading to dilated cardiomyopathy in 9-50% of cases and sudden death in 2.7-10%, or else manifest as pancarditis, with a mortality rate as high as 40% [45, 46, 47, 48, 49].
Incidence of tuberculous pericarditis is estimated between 1 and 4%, with a mortality rate of 90% without medical care versus 12% if timely diagnosed and adequately treated [50]. Since the Bacillus Calmette-Guérin (BCG) vaccine, developed in 1906, was only licenced for human use in 1921, and streptomycin was first used shortly after the Second World War in 1946, tuberculous pericarditis was a prevalent life-threatening disease [51, 52]. Nowadays, it occurs less frequently with exuberant clinical symptoms and fatal outcome, except in the context of immunosuppression [53, 54, 55].
Other causes of pericardial disease were progressively identified and linked to the relevant morphological pattern such as fibrinous pericarditis (also known as “bread and butter” pericarditis) in viral infections and autoimmune disorders following myocardial infarction or chronic renal failure (uraemic) [56, 57, 58, 59]. Despite improvements in renal replacement therapy, pericardial involvement may still occur in the setting of previously undiagnosed advanced kidney disease or when patients are ineffectively dialysed [60].
Ventricular aneurysms are usually complications of several diseases, namely cardiac infections, chest trauma or ischaemic myocardial scarring/deformation [61, 62, 63, 64]. This last scenario is of utmost importance, since out-of-hospital cardiac arrest due to ischaemic heart disease accounts for 50-60% of cases [64]. Left ventricle aneurysms in ischaemic hearts occur in 4-20% of cases, 85% of which are anterior, with apical and/or septal involvement [65, 66, 67, 68]. Associated mortality may result from thromboembolism, heart failure, rupture or arrhythmias [67].
This museological survey highlights the relevance of pathology museums and their impressive collections, which offer a unique glimpse into the past of cardiovascular pathology and a documentation of diseases currently ranking first in overall mortality rates in the Western world.


The authors pay homage to Professor Renato Trincão (1920-1996), who was Full Professor of Pathological Anatomy at the Faculty of Medicine of Coimbra University, Director of the Institute of Anatomical Pathology until 1990, and a keen promoter of the museum. The authors also wish to convey gratitude to the staff of the Pathology Museums of Coimbra and Florence Universities.
The authors declare no conflict of interest.


1. Oxford Dictionaries [cited 2018 Sep 30]. Available from: https://en.oxforddictionaries.com/definition/wax
2. Nature.com [cited 2018 Sep 30]. Available from: https://www.nature.com/subjects/waxes
3. Cooke RA. A moulage museum is not just a museum. Wax models as teaching instruments. Virchows Arch 2010; 457: 513-520.
4. Ballestriero R. Anatomical models and wax Venuses: art masterpieces or scientific craft works? J Anat 2010; 216: 223-234.
5. Pastor JF, Gutiérrez B, Montes JM, Ballestriero R. Uncovered secret of a Vasseur-Tramond wax model. J Anat 2016; 228: 184-189.
6. Nesi G, Santi R, Taddei GL. Art and the teaching of pathological anatomy at the University of Florence since the nineteenth century. Virchows Arch 2009; 445: 15-19.
7. Marinkoviæ S, Laziæ D, Kanjuh V, et al. Heart in anatomy history, radiology, anthropology and art. Folia Morphol 2014; 73: 103-112.
8. Paluchowski P, Gulczyñski J, Szarszewski A, et al. Insight into the history of anatomopathological museums = Part 1. From casual assemblages to scientific collections. Pol J Pathol 2016; 67: 207-215.
9. Gulczyñski J, Paluchowski P, Halasz J, et al. An insight into the history of anatomopathological museums. Part 2. Pol J Pathol 2018; 69: 118-127.
10. Mitchell SC, Korones SB, Berendes HW. Congenital heart disease in 56.109 births. Incidence and natural history. Circulation 1971; 43: 323-332.
11. Samánek M. Children and congenital heart disease: probability of natural survival. Pediatr Cardiol 1992; 13: 152-158.
12. van der Bom T, Zomer C, Zwinderman AH, et al. The changing epidemiology of congenital heart disease. Nat Rev Cardiol 2011;8:50-60.
13. Angelini A, di Gioia C, Doran H, et al. Association for European Cardiovascular Pathology (AECVP). Virchows Arch 2020; 476: 797-820.
14. Gómez O, Martínez M, Olivella A, et al. Isolated ventricular septal defects in the era of advanced fetal echocardiography: risk of chromosomal anomalies and spontaneous closure rate from diagnosis to age of 1 year. Ultrasound Obstet Gynecol 2014; 43: 65-71.
15. Cresti A, Giordano R, Koestenberger M, et al. Incidence and natural history of neonatal isolated ventricular septal defects: do we know everything? A 6-year single-center Italian experience follow-up. Congenit Heart Dis 2018; 13: 105-112.
16. Buratto E, Ye X-T, Konstantinov IE. Simple congenital heart disease: a complex challenge for public health. J Thorac Dis 2016; 8: 2994-2996.
17. Fernandes SM, Pearson DD, Rzeszut A, et al. Adult congenital heart disease incidence and consultation: a survey of general adult cardiologists. JACC 2013; 61: 1303-1304.
18. Benziger CP, Stout K, Zaragoza-Macias E, et al. Projected growth of the adult congenital heart diease population in the United States to 2050: an integrative systems modeling approach. Popul Health Metr 2015; 13: 29.
19. Afilalo J, Therrien J, Pilote L, et al. Geriatric congenital heart disease. Burden of disease and predictors of mortality. JACC 2011; 58: 1509-1515.
20. Corno A, Becker AE, Bulterijs AHK, et al. Univentricular heart: can we alter the natural history? Ann Thorac Surg 1982; 34: 716-727.
21. Frescura C, Thiene G. The new concept of univentricular heart. Front Pediatr 2014; 2: 62.
22. Corno AF. Univentricular heart. Front Pediatr 2015; 3: 75.
23. de Gouveia RH. Senac, Jean-Baptiste de (1693-1770). In: van den Tweel JG (eds) Pioneers in Pathology. Encyclopedia of Pathology. Spinger, Cham 2017; 482-483.
24. Murphy ML, White HJ, Meade J, Straub KD. The relationship between hypertrophy and dilatation in the postmortem heart. Clin Cardiol 1988; 11: 297-302.
25. Basso C, Aguilera B, Banner J, et al. Guidelines for autopsy investigation of sudden cardiac death: 2017 update from the Association for European Cardiovascular Pathology. Virchows Arch 2017; 471: 691-705.
26. Braunwald E. Lawbrew CT, Rockoff SD, et al. Idiopathic hypertrophic subaortic stenosis. 1. A description of the disease based upon an analysis of 64 patients. Circulation 1964; 30 (Suppl 4): 3-119.
27. Hypertrophic obstructive cardiomyopathy. Br Med J 1966; 1: 2-3.
28. Abecasis J, Gouveia R, Castro M, et al. Surgical pathology of subaortic septal myectomy: histology skips over clinical diagnosis. Cardiovasc Pathol 2018; 33: 32-38.
29. Maron BJ, Pelliccia A. The Heart of Trained Athletes. Cardiac remodeling and the risks of sports, including sudden death. Circulation 2006; 114: 1633-1644.
30. Hindieh W, Adler A, Weissler-Snir A, et al. Exercise in patients with hypertrophic cardiomyopathy: a review of current evidence, national guideline recommendations and a proposal for a new direction to fitness. J Sci Med Sport 2017; 20: 333-338.
31. Zhang Y, Ren J. Epigenetics and obesity cardiomyopathy: From pathophysiology to prevention and management. Pharmacol Ther 2016; 161: 52-66.
32. Fontes-Carvalho R, Fontes-Oliveira M, Sampaio F, et al. Influence of epicardial and visceral fat on left ventricular diastolic and Systolic Functions in Patients After Myocardial Infarction. Am J Cardiol 2014; 114: 1663-1669.
33. Quain R. On fatty diseases of the heart. Med Chir Trans 1850; 33: 121-196.
34. de Gouveia RH, Ferreira T, d’Aguiar MJ, et al. Quain’s Fatty Heart. Virchows Arch 2017; 471 (Suppl 1): S42-S43.
35. Bruce Fye W. Jean François Fernel. Clin Cardiol 1997; 20: 1037-1038.
36. Millar BC, Moore JE. Emerging issues in infective endocarditis. Emerg Infect Dis 2004; 10: 1110-1116.
37. Geller SA. Infective endocarditis: a history of the development of its understanding. Autops Case Rep 2013; 3: 5-12.
38. Aminov RI. A brief history of the antibiotic era: lessons learned and challenges for the future. Front Microbiol 2010; 1: 134.
39. Fernández Guerrero ML, Álvarez B, Manzarbeitia F, Renedo G. Infective endocarditis at autopsy: a review of pathologic manifestations and clinical correlates. Medicine (Baltimore) 2012; 91: 152-164.
40. Pilmis B, Mizrahi A, Laincer A, et al. Infective endocarditis: Clinical presentation, etiology, and early predictors of in-hospital case fatality. Med Mal Infect 2016; 46: 44-48.
41. Iung B, Vahanian A. Epidemiology of acquired valvular heart disease. Can J Cardiol 2014; 30: 962-970.
42. Garcia-Albéniz, Hsu J, Lipsitch M, et al. Infective endocarditis and cancer in the elderly. Eur J Epidemiol 2016; 31: 41-49.
43. Fernández-Cruz A, Mu¼oz P, Sandoval C, et al. Infective endocarditis in patients with cancer: a consequence of invasive procedures or a harbinger of neoplasm? A prospective, multicenter cohort. Medicine 2017; 96: 38-46.
44. Castonguay MC, Burner KD, Edwards WD, et al. Surgical pathology of native valve endocarditis in 310 specimens from 287 patients (1985-2004). Cardiovasc Pathol 2013; 22: 19-27.
45. de Gouveia RH, Corte Real Gonçalves FMA. Sudden cardiac death and valvular pathology. Forensic Sci Res 2019; 4: 280-286.
46. Kindermann I, Barth C, Mahfound F, et al. Update on myocarditis. J Am Coll Cardiol 2012; 59: 779-792.
47. Fung G, Luo H, Qiu Y, et al. Myocarditis. Circ Res 2016; 118: 496-514.
48. Bracamonte-Baran W. Cardiac autoimmunity: myocarditis. Adv Exp Med Biol 2017; 1003: 187-221.
49. Yoon JK, Rahimi MB, Fiore A, et al. Bacterial pancarditis with myocardial abscess. Tex Heart Inst J 2015; 42: 55-57.
50. Echeverri D, Matta L. Pericarditis tuberculosa [Tuberculous pericarditis]. Biomedica 2014; 34: 528-534.
51. Calmette A. Preventive vaccination against tuberculosis awith BCG. Proc R Soc Med 1931; 24: 1481-1490.
52. Cooke RE, Dunphy DL, Blake FG. Streptomycin in tuberculous meningitis; a report of its use in a one-year-old infant. Yale J Biol Med 1946; 18: 221-226.
53. Luft FC, Rissing JP, White A, Brooks GF. Infections or neoplasm as causes of prolonged fever in cancer patients. Am J Med Sci 1976; 272: 65-74.
54. Barreto ML, Pérez J. Pericarditis por Mycobacterium tuberculosis multiresistente en un paciente con infección por VIH. Reporte de un caso clínico y revision de la literature. Rev Chil Infect 2009; 26: 156-161.
55. Ntsekhe M, Mayosi BM. Tuberculous pericarditis with and without HIV. Heart Fail Rev 2013; 18: 367-373.
56. Cohen MB. Cross your heart: some historical comments about fibrinous pericarditis. Hum Pathol 2004; 35: 147-149.
57. de Gouveia RH. Corvisart, Jean Nicolas (1755-1821). In: van den Tweel JG (eds) Pioneers in Pathology. Encyclopedia of Pathology. Spinger, Cham 2017; 109-110.
58. de Gouveia RH, Santos C, Santi R, Nesi G. Lessons from the past: uremic pericarditis. Cor Vasa 2018; 60: e101-e103.
59. Sadjadi S-A, Mashhdian A. Uremic pericarditis: a report of 30 cases and review of the literature. Am J Case Rep 2015: 16: 169-173.
60. Dad T, Sarnak MJ. Pericarditis and pericardial effusions in end-stage renal disease. Semin Dial 2016; 29: 366-373.
61. Carrilho-Ferreira P, Silva Marques J, Gouveia R, Brito D. Eosinophilic myocarditis with left ventricular apical aneurysm. Eur Heart J Cardiovasc Imaging 2014; 15: 228.
62. Grieco JG, Montoya A, Sullivan HJ, et al. Ventricular aneurysm due to blunt chest injury. Ann Thorac Surg 1989; 47: 322-329.
63. Lai W-T, Lin S-M, Wu S-J, et al. Post-traumatic left ventricular aneurysm with massive hemopericardium in a child presenting 3 years after a fall. Pediatr Neonatol 2013; 54: 406-408.
64. de Gouveia RH, Martins A, Vieira DN. Sudden death as the outcome of cardiac arrest, in a Portuguese region: where do resuscitation manoeuvres stand? WJCD 2015; 5: 227-232.
65. Vural KM, Şener E, Özatik MA, et al. Left ventricular aneurysm repair: an assessment of surgical treatment modalities. Eur J Cardiothorac Surg 1998; 13: 49-56.
66. Versteegh MIM, Lamb HJ, Bax JJ, et al. MRI evaluation of left ventricular function in anterior LV aneurysms before and after surgical resection. Eur J Cardiothorac Surg 2003; 23: 609-613.
67. Bechtel JFM, Tölg R, Graf B, et al. High incidence of sudden death late after anterior LV-aneurysm repair. Eur J Cardiothorac Surg 2004; 25: 807-811.
68. Zoffoli G, Mangino D, Venturini A, et al. Diagnosing left ventricular aneurysm from pseudo-aneurysm: a case report and a review in literature. J Cardiothorac Surg 2009; 4: 11-15.
Copyright: © 2022 Polish Association of Pathologists and the Polish Branch of the International Academy of Pathology This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Quick links
© 2022 Termedia Sp. z o.o. All rights reserved.
Developed by Bentus.