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THE ELECTROCARDIOGRAM IN MITRAL-VALVE DISEASE
1288 THE
ELECTROCARDIOGRAM IN MITRAL-VALVE DISEASE
THE electrocardiogram in disease of the mitral valve reflects the effects of the lesion primarilyon the left
atrium, and secondarily on the right ventricle (in pure or dominant stenosis) or the left ventricle (in dominant
incompetence). Appreciable left atrial enlargement and hypertension is reflected in the character of the P wave, which is widened and notched but of normal amplitlldé.1 This widening and notching is present in most severe cases of mitral stenosis in sinus rhythm, but not in slight cases.2 When pulmonary hypertension is present, the p wave may become augmented in amplitude, reflecting right atrial hypertension, and enlargement of both atria may be revealed by a tall, broadened, and notched p wave. Persistent atrial fibrillation, however, is present in roughly 45% of all cases of mitral-valve disease.2
The evidence therefore
suggests that critical mitral pulmonary arterial hypertension) can exist withbut’a corresponding degree of right ventricular dominance on the cardiogram. The presence of gross right ventricular dominance in mitral-valve disease virtually guarantees severe pulmonary arterial hypertension, but does not exclude mitral incompetence associated with stenosis.55 When there is cardiographic evidence of, abnormal left ventricular dominance, pure mitral stenosis cannot be the sole lesion, and dominant mitral-incompetence, aortic-valve disease, or severe systemic hypertension is likely. stenosis
(if
not
severe
TUBULAR DYSFUNCTION IN NEPHROSIS
RENAL biopsy in the nephrotic syndrome has shown that among the common renal lesions are subacute
glomerular nephritis (membranous
or
proliferative),
chronic glomerular nephritis, diabetic glomerulosclerosis, Since mitral stenosis is one of the commonest causes of in ventricular lupus nephritis (in systemic lupus erythematosus), thromhypertrophy right acquired heart-disease, bosis of the renal vein, and renal amyloidosis.11 But of 56 the cardiogram often shows evidence of this.3 The pulmonary arterial pressure and arteriolar resistance has4 cases investigated in this way, 6 are described as " neph-1 rotic syndrome with predominant tubular degeneration." been shown to be related to the left atrial pressure,4 This is interesting because it has become widely accepted and to the severity of the mitral stenosis.55 It might that in the nephrotic syndrome the primary lesion is globe supposed, therefore, that the degree of right ventricular hypertrophy apparent in the cardiogram would be a merular, causing increased filtration of protein, and that good guide to the severity of the mitral stenosis. Wood2 the heavy proteinuria is only partly or else not at all due to defective tubular reabsorption. Such histological changes noted that the degree of right ventricular hypertrophy as are present in the proximal tubular epithelium are was correlated closely with the height of the pulmonary related by some to maximal protein reabsorption; and arteriolar resistance, while Goodwin et awl. found poor between the of ventricular simple tests, such as measurement of specific-gravity range agreement degree right or p-aminohippurate excretion, show normal tubular dominance on the one hand and the size of the mitral function in most cases. valve or degree of pulmonary hypertension on the other ; The primary importance of a glomerular lesion in nephrobut Wood and Goodwin agreed that severe right ventrisis has now been challenged, however, by Freeman and cular dominance indicated a high pulmonary-arterial Joekes,2 who believe that there is " diminished tubular pressure and resistance and a small mitral valve. The association of augmented, pointed p waves without protein reabsorption, without necessarily any abnormal proportionate evidence of right ventricular dominance escape of protein through the glomeruli." By means of should suggest the possibility of associated tricuspid paper electrophoresis they studied the differential protein stenosis.s patterns in serum, urine, and oedema fluid of 6 nephrotic The difference in the findings in the two series of cases patients. The patterns were very similar in urine and oedema fluid, which both showed a much higher proportion may be explained by several factors. The electrocardioof albumin to globulin than did the serum. Freeman graphic assessment of the severity of right ventricular and Joekes reason that the abnormal quantities of plasmadominance is difficult. The degree of pulmonary hypertension was measured by cardiac catheterisation in lipoprotein and the consequent increase in the molecular size of the globulins led to a preferential loss of albumin Wood’s cases, but for the great part it was assessed radiologically in those of Goodwin et al. Moreover, associated into the tissue-spaces and renal tubules. Normal or raised ratios of serum-albumin to tissue-fluid-albumin in left ventricular hypertrophy may modify the picture 7 ; these patients appeared to exclude an increased escape Goodwin et al. claimed that some patients with critically of albumin due to a generalised capillary lesion. These stenosed valves had no evidence of any right ventricular are of interest, but the argument put forward and a third of these had left findings only hypertrophy, any ventricular hypertrophy. by Freeman and Joekes is by no means conclusive. Extreme right ventricular dominance is associated with Stanbury and Macaulay,3 who accept the glomerular lesion as primary, have recently discussed secondary renal tall delayed R waves, sometimes preceded by Q waves and tubular insufficiency in the nephrotic syndrome. Renal followed by inverted T waves, in right precordial leads, and deep s waves in left precordial leads. These findings glycosuria and amino-aciduria, either singly or together, have been reported in nephrotic patients, and Tegelaers are common in congenital heart-disease, such as puland Tiddens4 have described a more complex combinabut rare in ventricular monary stenosis, acquired right of tubular defects in 2 nephrotic children in whom tion that mitral accompanying hypertrophy, including renal glycosuria and amino-aciduria, acidosis, hypokalstenosis. 8 Morris and Whitaker9 reported 9 such cases in 173 patients with mitral stenosis ; and Pruitt and aemia, and polyuria developed. The rather similar patient described by Stanbury and Macaulay was first seen at 41 Robinson 1° found cases in 93 patients with severe the age of 2 years with all the typical clinical and biomitral stenosis, and 53 of extreme right ventricular chemical features of the nephrotic state and was treated dominance among 147 patients with mitral-valve disease with cortisone for a week, concentrated plasma infusions, of all types. low-salt and high-protein diet, and, for several months, 1. Wood, P. Diseases of the Heart and Circulation. London, 1950. cation-exchangeresin (’ Katonium ’). The nephrotic 2. Wood, P. Brit. med. J. 1954, i, 1051, 1113. state continued, but hypocalcaemic tetany developed 3. Trounce, J. R. Brit. Heart J. 1952, 14, 185. the patient was 4 years of age ; and subsequently when 4. Holling, H. E. Brit. med. Bull. 1952, 8, 358. he was found to have renal glycosuria and amino-aciduria, 5. Goodwin, J. F., Hunter, J. D., Cleland, W. P., Davies, L. G., which had not been present at the onset of his illness. Steiner, R. E. Brit. med. J. 1955, ii, 573. 6. Gibson, R., Wood, P. Brit. Heart J. 1955, 17, 552. 7. Pagnoni, A., Goodwin, J. F. Ibid, 1952, 14, 451. 8. Campbell, M. Ibid, p. 204. 9. Morris, T. L., Whitaker, W. Amer. Heart J. 1956, 52, 738. 10. Pruitt, R. D., Robinson, J. G. Ibid, p. 880.
1. 2. 3. 4.
Kark, R. M. Cited by Findley, T. Amer. Heart J. 1957, 53, 323. Freeman, T., Joekes, A. M. Acta med. scand. 1957, 157, 43. Stanbury, S. W., Macaulay, D. Quart. J. Med. 1957, 26, 7. Tegelaers, W. H., Tiddens, H. W. Helv. pœdiat. Acta, 1955, 10, 269.
ELECTROCARDIOGRAM IN MITRAL-VALVE DISEASE
THE electrocardiogram in disease of the mitral valve reflects the effects of the lesion primarilyon the left
atrium, and secondarily on the right ventricle (in pure or dominant stenosis) or the left ventricle (in dominant
incompetence). Appreciable left atrial enlargement and hypertension is reflected in the character of the P wave, which is widened and notched but of normal amplitlldé.1 This widening and notching is present in most severe cases of mitral stenosis in sinus rhythm, but not in slight cases.2 When pulmonary hypertension is present, the p wave may become augmented in amplitude, reflecting right atrial hypertension, and enlargement of both atria may be revealed by a tall, broadened, and notched p wave. Persistent atrial fibrillation, however, is present in roughly 45% of all cases of mitral-valve disease.2
The evidence therefore
suggests that critical mitral pulmonary arterial hypertension) can exist withbut’a corresponding degree of right ventricular dominance on the cardiogram. The presence of gross right ventricular dominance in mitral-valve disease virtually guarantees severe pulmonary arterial hypertension, but does not exclude mitral incompetence associated with stenosis.55 When there is cardiographic evidence of, abnormal left ventricular dominance, pure mitral stenosis cannot be the sole lesion, and dominant mitral-incompetence, aortic-valve disease, or severe systemic hypertension is likely. stenosis
(if
not
severe
TUBULAR DYSFUNCTION IN NEPHROSIS
RENAL biopsy in the nephrotic syndrome has shown that among the common renal lesions are subacute
glomerular nephritis (membranous
or
proliferative),
chronic glomerular nephritis, diabetic glomerulosclerosis, Since mitral stenosis is one of the commonest causes of in ventricular lupus nephritis (in systemic lupus erythematosus), thromhypertrophy right acquired heart-disease, bosis of the renal vein, and renal amyloidosis.11 But of 56 the cardiogram often shows evidence of this.3 The pulmonary arterial pressure and arteriolar resistance has4 cases investigated in this way, 6 are described as " neph-1 rotic syndrome with predominant tubular degeneration." been shown to be related to the left atrial pressure,4 This is interesting because it has become widely accepted and to the severity of the mitral stenosis.55 It might that in the nephrotic syndrome the primary lesion is globe supposed, therefore, that the degree of right ventricular hypertrophy apparent in the cardiogram would be a merular, causing increased filtration of protein, and that good guide to the severity of the mitral stenosis. Wood2 the heavy proteinuria is only partly or else not at all due to defective tubular reabsorption. Such histological changes noted that the degree of right ventricular hypertrophy as are present in the proximal tubular epithelium are was correlated closely with the height of the pulmonary related by some to maximal protein reabsorption; and arteriolar resistance, while Goodwin et awl. found poor between the of ventricular simple tests, such as measurement of specific-gravity range agreement degree right or p-aminohippurate excretion, show normal tubular dominance on the one hand and the size of the mitral function in most cases. valve or degree of pulmonary hypertension on the other ; The primary importance of a glomerular lesion in nephrobut Wood and Goodwin agreed that severe right ventrisis has now been challenged, however, by Freeman and cular dominance indicated a high pulmonary-arterial Joekes,2 who believe that there is " diminished tubular pressure and resistance and a small mitral valve. The association of augmented, pointed p waves without protein reabsorption, without necessarily any abnormal proportionate evidence of right ventricular dominance escape of protein through the glomeruli." By means of should suggest the possibility of associated tricuspid paper electrophoresis they studied the differential protein stenosis.s patterns in serum, urine, and oedema fluid of 6 nephrotic The difference in the findings in the two series of cases patients. The patterns were very similar in urine and oedema fluid, which both showed a much higher proportion may be explained by several factors. The electrocardioof albumin to globulin than did the serum. Freeman graphic assessment of the severity of right ventricular and Joekes reason that the abnormal quantities of plasmadominance is difficult. The degree of pulmonary hypertension was measured by cardiac catheterisation in lipoprotein and the consequent increase in the molecular size of the globulins led to a preferential loss of albumin Wood’s cases, but for the great part it was assessed radiologically in those of Goodwin et al. Moreover, associated into the tissue-spaces and renal tubules. Normal or raised ratios of serum-albumin to tissue-fluid-albumin in left ventricular hypertrophy may modify the picture 7 ; these patients appeared to exclude an increased escape Goodwin et al. claimed that some patients with critically of albumin due to a generalised capillary lesion. These stenosed valves had no evidence of any right ventricular are of interest, but the argument put forward and a third of these had left findings only hypertrophy, any ventricular hypertrophy. by Freeman and Joekes is by no means conclusive. Extreme right ventricular dominance is associated with Stanbury and Macaulay,3 who accept the glomerular lesion as primary, have recently discussed secondary renal tall delayed R waves, sometimes preceded by Q waves and tubular insufficiency in the nephrotic syndrome. Renal followed by inverted T waves, in right precordial leads, and deep s waves in left precordial leads. These findings glycosuria and amino-aciduria, either singly or together, have been reported in nephrotic patients, and Tegelaers are common in congenital heart-disease, such as puland Tiddens4 have described a more complex combinabut rare in ventricular monary stenosis, acquired right of tubular defects in 2 nephrotic children in whom tion that mitral accompanying hypertrophy, including renal glycosuria and amino-aciduria, acidosis, hypokalstenosis. 8 Morris and Whitaker9 reported 9 such cases in 173 patients with mitral stenosis ; and Pruitt and aemia, and polyuria developed. The rather similar patient described by Stanbury and Macaulay was first seen at 41 Robinson 1° found cases in 93 patients with severe the age of 2 years with all the typical clinical and biomitral stenosis, and 53 of extreme right ventricular chemical features of the nephrotic state and was treated dominance among 147 patients with mitral-valve disease with cortisone for a week, concentrated plasma infusions, of all types. low-salt and high-protein diet, and, for several months, 1. Wood, P. Diseases of the Heart and Circulation. London, 1950. cation-exchangeresin (’ Katonium ’). The nephrotic 2. Wood, P. Brit. med. J. 1954, i, 1051, 1113. state continued, but hypocalcaemic tetany developed 3. Trounce, J. R. Brit. Heart J. 1952, 14, 185. the patient was 4 years of age ; and subsequently when 4. Holling, H. E. Brit. med. Bull. 1952, 8, 358. he was found to have renal glycosuria and amino-aciduria, 5. Goodwin, J. F., Hunter, J. D., Cleland, W. P., Davies, L. G., which had not been present at the onset of his illness. Steiner, R. E. Brit. med. J. 1955, ii, 573. 6. Gibson, R., Wood, P. Brit. Heart J. 1955, 17, 552. 7. Pagnoni, A., Goodwin, J. F. Ibid, 1952, 14, 451. 8. Campbell, M. Ibid, p. 204. 9. Morris, T. L., Whitaker, W. Amer. Heart J. 1956, 52, 738. 10. Pruitt, R. D., Robinson, J. G. Ibid, p. 880.
1. 2. 3. 4.
Kark, R. M. Cited by Findley, T. Amer. Heart J. 1957, 53, 323. Freeman, T., Joekes, A. M. Acta med. scand. 1957, 157, 43. Stanbury, S. W., Macaulay, D. Quart. J. Med. 1957, 26, 7. Tegelaers, W. H., Tiddens, H. W. Helv. pœdiat. Acta, 1955, 10, 269.