Welcome back to our fascinating journey via the historical course of Pediatric cardiology.

It would be unjust not to write more about the towering figure of Thomas Bevill Peacock. No other name appears with such consistency as this in the monumental textbook called “Clinical Recognition of Congenital Heart Diseases” by Joseph K Perloff. Dr Perloff’s eye for historical details is a phenomenon by itself. That naturally endears the reverence for Thomas Peacock.

Thomas Peacock was writing in an era when Cardiology was gaining grounds. The first authentic English text in Cardiology was published in AD 1809 by Allan Burns of Glasgow. It was titled, “Observations on some of the most Frequent and Important Diseases of the Heart”. He gave neat and clear descriptions of cardiac murmurs. His classification of the heart disease was in three categories: (1) Sympathetic, deriving from other organs of the body, (2) 'Malformations' or Congenital defects, and (3) Organic diseases of the heart. Peacock’s contemporaries also included people like Stokes, Graves, Corrigan and Cheyne who extended the knowledge of physical signs and revived interest in treatment of heart ailments.

Peacock’s inspiration for heart ailments and motivation to write about them probably came from two contemporaries of his: James Hope, who in AD 1831 published “A Treatise on the Diseases of the Heart and Great Vessels” and Peter Latham, who was a known authority on Rheumatic Heart Disease. Latham’s “Lectures on Subjects Connected with Clinical Medicine Comprising Diseases of the Heart” published in AD 1845 remains both epigrammatic and entertaining. Between AD 1846 and AD 1862, Peacock worked on Cardiology related issues. His works spread across: Dissecting aneurysm of aorta, Valvular heart disease, Congenital heart disease, and Measurements of the normal and diseased heart.

Peacock’s Magnum Opus was published in AD 1858 and was titled, “On Malformations of the Human Heart”. The book started as a compilation of series of lectures that he gave to the students of St. Thomas's Hospital in AD 1854. The era had evoked a great interest on Congenital Heart Disease. Hence, he published them in the Medical Times and Gazette which had a great response from medical fraternity. After careful revision and greater elaboration, he produced the book. The period had an incomplete anatomical and physiological knowledge on the subject. One can imagine problem of classifying the many unexplained defects that were being set up in to an orderly arrangement. For example, the cause of cyanosis was completely unknown at that time and as previously described (see the previous post), Peacock held a strong opposition to the admixture of blood as the cause of cyanosis. He had firmly believed that the cyanosis was due to venous stasis and obstruction to the flow. Peacock came up with a novel idea to solve the problem of classification: He combined an anatomical with embryological classification. This is very evident from the book’s “Table of Contents”.

His account of “Fallot’s Tetralogy”, 42 years prior to Fallot’s description is indeed interesting. It goes something like this:
MALFORMATION OF THE HEART, CONSISTING IN CONTRACTION OF THE ORIFICE OF THE PULMONARY ARTERY WITH DEFICIENCY AT THE BASE OF THE INTERVENTRICULAR SEPTUM.
In this case there existed extreme contraction of the orifice of the pulmonary artery, with a deficiency in the interventricular septum, and the aorta arose in chief part from the right ventricle. The right auricle and ventricle were of large size, and the walls of the latter thick and very firm. The left ventricle was, on the contrary, small, and its walls thin and flaccid. The left auricle was also small. The foramen ovale and ductus arteriosus were both closed. The heart was taken from a child two years and five months old, who had exhibited well-marked symptoms of cyanosis, which commenced three months after birth. It was remarked that though the recorded cases are numerous in which, with more or less contraction of the orifice of the pulmonary artery, the septum of the ventricles is found deficient, it is far from frequent to meet with these malformations, with, as in the present instance, a closed state of the foramen ovale; and especially so, when the degree of contraction of the pulmonary artery is extreme. The intensity of the cyanosis, and the duration of life in these cases, bears a general relation to the amount of contraction of the pulmonary orifice and the freedom of communication between the right and left cavities of the heart, through the medium of the open foramen ovale and the aperture in the interventricular septum. Dr. Peacock, 7th of December, 1846.

Peacock makes many interesting observations: the difference between valvular and infundibular type of pulmonary stenosis, pulmonary valves often becoming the seat of subsequent disease, “and display recent deposits or vegetation . .. in some cases, indeed, the obstruction is mainly due to warty growths from the valves”.
Peacock also noticed the susceptibility of congenitally abnormal aortic and pulmonary valves to chronic inflammatory changes.

In 186o, Peacock reported a case to the Pathological Society, which had the features of Infective Endocarditis. The comments at the end of the report reads as following:
The great interest of the case Dr. Peacock considered to be:
1. The existence of disease both in the aortic and mitral valves, which had been manifested by distinct physical signs, so that a correct diagnosis had been effected during life.
2. The musical character of the murmur heard at the base with the diastole of the heart, and which was clearly traceable to the loose retroverted edge of the posterior semilunar valve.
The great concern with which the physical signs can lead to a correct anatomical diagnosis without any mention of the etiological possibilities is the point of concern here, considering the time when etiological diagnosis was not easy.

Peacock’s contribution to Valvular heart disease was equally noteworthy. However, it should be noted that Peacock was not an exclusive cardiac physician. He was more of a general physician with special interest in pathological anatomy. His name remains remembered even today in Cardiology for his exhaustive observations, deep interest in understanding the new concepts, the orderly fashion in which he arranges the details and his beautiful and masterly illustrations. In Maude Abbott’s words, “The first comprehensive study, covering the whole field and reviewing the earlier literature may be said to be Peacock's, which remains a classic and is still the leading authority in English upon the subject”. Considering Abbott’s contribution to this field, these words stand as the testimony of Peacock’s contribution to the subject of Pediatric Cardiology.

The end of Thomas Peacock was probably as he wished for it: on 30 May 1882, at the age of 70 years. It happened in the St. Thomas's Hospital, which he had served for 28 years and had retired as the Dean. After having attended a lecture by James Paget, he was accompanying some friends, to whom he was proudly showing the hospital. “He fell down in one of the corridors and was carried into the ward to which he had formerly been physician, and died that same evening in the very place which probably in health he would have chosen to die.” It was probably the way our ancient Indian seers wished to end the present journey of life. Peacock was a seer in all the respects, including the end.

(Ref:
Peacock TB. On Malformations of the Human Heart. London, J. Churchill, 1858.

ABBOTT, M. E. Congenital cardiac disease. In Osler, Sir William, Modern Medicine, vol. IV, Philadelphia and New York, Lea and Febiger, 1908.

Malformation of the heart, consisting in contraction of the orifice of the pulmonary artery with deficiency at the base of the interventricular septum.
Trans. path. Soc. Lond., 1846:8;52

Malformation of the heart. Stenosis at the commencement of the conus arteriosus of the right ventricle and at the origin of the pulmonary artery; aperture in septum ventriculorum and aorta arising partly from right side; foramen ovale and ductus arteriosus closed. Cyanosis. Trans. path. Soc. Lond., 1875-6, 27, 131-6

Retroversion of one of the aortic valves, and destruction of some of the chordae tendinaea of the mitral valve. Ibid., 59-61

BRISTOW, J. S. Obituary of Dr. T. B. Peacock. St. Thos. Hosp. Rep., 1882, 12, 1, 79

Flaxman, N. Peacock and congenital heart disease. Bull. Hist. Med., 1939:7;1061-1103)

Next time, we shall see further progress of the field in 19th century.

On a personal note, it was a pleasant surprise for me when the issue of this blog was discussed in one of our academic sessions. The ever-dependable Dr Vishal Changela (who also happens to be one of the very first followers of this blog), vehemently and passionately advertised my blog to the team in words, which I could probably not have bettered. His rhetoric was so convincing and pressing that the blog had many new visitors and few new followers. I also got the suggestion to post-script all my email communications with the blog id. It is indeed a good thing. Hope the list of people who read this blog grows!

How to approach an infant with ASD, Ebstenoid TV and PDA, in which the PDA shunts bi-directional? Even when infant desaturates a bit, closing PDA should not be a problem, as ASD can still tackle the PAH. Is there a role of cath study for operability? Our team had a split opinion on this. What is your take? Please send them.

Does {S,D,L} DORV with subaortic VSD always needs a homograft? On Echo, it looks as if routing the VSD to Aorta would solve the problem. But the surgeons, (who would obviously think in 3D) feel that doing such a thing would isolate PA from RV. This is because the aorta is anterior and the patch closing VSD would come in the way of RV to PA path. Anyone has any experience in this regard? Please let me know.

In refractory VF, how many DC shocks are permitted? I don’t know if there is a fixed upper limit. The objective would be to save the patient rather than count the numbers! However, we had an interesting discussion on this today, brought up by our fellow, Dr Karunakar.
As per the PALS guidelines, 3 shocks are mentioned. What if patient does not revert with this? There are always instances of multiple shocks, nearly charring the skin of patient, but successfully defibrillating and saving the patient at the end. Is the issue ethical if the effort finally makes the patient survive? Let me know your take on it.

Thanks to our new followers: Dr Raghunath is our senior pediatric Intensivist, trained at Australia. He has been instrumental in formulating the PITU protocols along with the other colleagues of his team.
Dr Amit Misri is a senior member of our team; very skillful and dependable. To be short about him, he is an asset to any establishment he belongs to!

Advanced wishes to Dr Anamika, who would be presenting “Usual device; Unusual heart” tomorrow in the CSI meet. Also, thanks for her wise comments on the blog.

Please send in you inputs. For all the new followers, if you find any problem in posting your comments, please email them to me. I shall post it on your behalf.

Regards

Kiran