ered a recurrence rather than a relapse, as relapses tend to occur within two to four weeks after discontinuation of therapy. Additionally, this repeat episode coincided precisely with the reuse of parenteral heroin after clinical cure had been affected. Though phage typing of the organism was not done, the serum minimal inhibitory concentration level was distinctly greater during the sixth episode, 2 mEq methicillin/ml vs 16 mEq/ml. In summary, this case emphasizes two distinct and important points. First, recurrent infective endocarditis is most frequently encountered in parenteral drug abusers and may lead to progressive destruction of valve structures with ultimate death. This patient, indeed, required prosthetic aortic valve replacement during his third episode of endocarditis and died with multiple aortic ring abscesses and a fenestrated mitral valve. The second important point is that appropriately timed surgical intervention in patients with active infective endocarditis may not only result in a bacteriologic cure when resistant or persistent infections are present, but will prevent relentless hemodynamic compromise from continued valve destruction. This patient epitomizes the usually fatal clinical course of individuals developing recurrent infective endocarditis. ACKNOWLEDGMENTS: The authors wish to express their ajl~reciation to Dr. Han-Seob Kim for his help with tl!e_p'athology specimen, and to Mrs. Jeannie Ford for her sIdlIful secretarial assistance. REFERENCES
1 Welton DE, Young JB, Genby LO, et a1: Recurrent infective endocarditis: Analyses of predisposing factors and clinical features. Am J Med 66:932-938, 1979 2 Cherubin CE, Nev HC: Infective endocarditis at the Presbyterian Hospital in New York City: 1938-1967. Am J Med 51:83-96, 1971 3 Finland M, Barnes MW: Changing etiology of bacterial endocarditis in the antibacterial era. Ann Intern Med 72:341-348, 1970 4 Rabinovitch S, Evans J, Smith RM, et a1: A long-term view of bacterial endocarditis. Ann Intern Med 63:185198, 1965 5 Levison ME, Kay D, Mandell GH, et at: Characteristics of patients with multiple episodes of bacterial endocarditis. JAMA 211: 13i5-1357, 1970 6 Pelletier IL, Petersdorf RG: Infective endocarditis: A review of 148 cases. Medicine 56:287-313, 1977 7 Richardson IV, Karp RB, Kirldin JW, et at: Treabnent of infective endocarditis: A 10-year comparative analysis. Circulation 58:4:589-597, 1978 8 Rapaport E: The changing role of surgery in the management of infective endocarditis (editorial) . Circulation 58:4:598~99, 1978 9 Wilson WR, Danielson JK, Giviani ER, et at: Valve replacement in patients with acute infective endocarditis. Circulation 58:4:585-588, 1978 10 Young JB, Welton DE, Raizner AE, et aI: Surgery in active infective endocarditis. Circulation, in press 11 Kaye D (ed): Infective Endocarditis. Baltimore, UDiversity Park Press, 1976, p 198 12 GrifBn FM, Jones G, Cobbs CG, et at: Aortic insWBciency 76:23-28, 1972 in bacterial endocarditis. Ann Intern
584 ANZAI ET AL
Ruptured Aneurysm of Aortic Sinus of Valsalva into Right Ventricle* Nobuyuki Anzai, M.D.; Manabu Yamada, M.D.; Naofumi Fijii, M.D.; Yoichiro Kazama; M.D.; and Sosuke Miyazawa, M.D.
We report a patient with ruptured aneurysm of the aortic sinus of Valsalva into the right ventricle, whose heart murmur represented only a diastoUc element without aortic regurgitation. Surgery revealed a small opening through myocardium of the ventricular septum without ventricular septal defect. During systole, the opening w. constricted and presumably closed with myocardial contraction, and left-to-right shunt might have occurred only in diastole. This might lead to only a diastolic murmur.
he murmur of ruptured aneurysm of the aortic sinus of Valsalva into the right heart is frequently continuous or to and fro. We have encountered a patient with ruptured aneurysm of the aortic sinus of Valsalva into the right ventricle, whose heart murmur was heard only during diastole without aortic regurgitation. We describe the mechanism of this unusual manifestation of heart murmur. CASE REPORT
The patient was 21-year-old man who had been healthy until the end of March, 1975, when he noticed a heart murmur. He was referred to the Higashi Nagano National Hospital with the chief complaint of palpitation and precordial distress on May 16, 1975. On admission, his height was 170 em and weight 62 kg. His pulse rate was 94 beats/min and regular. His blood pressure was 128/50 mm Hg, On auscultation, a grade 2/6 diastolic murmur, loudest at the 2nd, 3rd and 4th intercostal spaces along the left sternal border, was heard (Fig 1). A thrill was also palpable at the same area. No abnormality was noted on examination of blood, urine, or tests of hepatic and renal function. The chest x-ray film showed moderately increased pulmonary blood flow, with a cardiothoracic ratio of 49 percent. The electrocardiographic findings revealed the following: regular sinus rhythm; P-R interval 0.14 sec; QRS axis + 60 0 ; no evidence of left or right ventricular hypertrophy. Right cardiac catheterization disclosed that oxygen saturation was increased in the right ventricle. The left-to-right shunt was 58 percent. During left cardiac catheterization, venbicular tachycardia occurred. Left ventricular pressure was difficult to obtain. (Table 1). Retrograde aortography revealed regurgitation of the contrast medium from the right coronary sinus into the outHow tract of the right ventricle without aortic regurgitation (Fig 2). The patient underwent surgery on May 5, 1975. An aneurysmal mass, 1 em in diameter and 1 em in length, was seen at the right ventricular outflow tract about 1 em beneath the pulmonic valve. The mass was incised at the base. This resulted in a defect of·the sinus wall approximately 3 mm in diameter. The opening was °From the Department of Cardiology and Cardiac Surgery, Higashi Nagano National Hospital, Nagano City, Japan. Reprint requests: Dr. Anzai, Department of Cardiology, Higashi Nagano National Hospital, 2-477 Uwano, Nagano
City, Japan 380
CHEST, 76: 5, NOVEMBER, 1979
L. 2 r.c.s,
L. 3 i.c.s,
L. _ 1.e.S.
1. Phonocardiogram demonstrating only diastolic element without systolic element.
closed with a patch suture. The ventricular defect was not found and the ventricular septum was intact. The postoperative course was uneventful. The disastoJic murmur disappeared. Postoperative x-ray examination revealed a reduction in size of the cardiac shadow, with the cardiothoracic ratio 38 percent, without relapse of the aneurysm. Table I-Dala /rom Inlnreartliae Cat1aeteri:mlion Oxygen
MaximumfMinimum pressure, mm Hg
Superior vena cava
Inferior vena cava
Right atrium Upper Middle Lower
20/8 (16) 22/9 (15) 22/8 (15)
70.0 66.4 68.4
Right ventricle Outflow Apex Inflow
50/5 (30) 60/0 (30) 60/5 (30)
85.8 96.5 85.8
Pulmonary artery Wedge Branch Main
14/7 (9) 40/20 (32) 60/20 (36)
89.7 84.5 83.0
CHEST, 76: 5, NOVEMBER, 1979
FIGURE 2. Lateral view of retrograde aortogram demonstrating regurgitation of contrast media from the right coronary sinus into the outflow tract of the right ventricle without aortic regurgitation.
The murmur of ruptured aneurysm of aortic sinus of Valsalva into the right heart frequently shows continuous or to-and-fro motion. l•2 The character of the murmur, however, depends upon the size of the aneurysm and fistulous tract, magnitude of left-to-right shunt, site of opening, associated congenital lesions and severity of cardiac failure.l,s-s Therefore, the murmur is not always continuous or to and fro. In cases of a small opening, only a systolic murmur is manifested, simulating an unruptured aneurysm in which only a systolic murmur is heard.8 , 1 In the ruptured aortic aneurysm of the sinus of Valsalva into the right heart, the continuous murmur is frequently accentuated in the diastolic element.l , 2 This diastolic accentuation is similar to that of a coronary A-V fistula, in which coronary blood flow is augmented during diastole and heart murmur is accentuated in diastole,"
Anatomic and hemodynamic similarity exists between a coronary artery, a coronary A-V fistula and a ruptured aortic aneurysm of sinus of Valsalva into the right ventricle." Anatomically, they originate in the aortic sinuses and terminate in the right heart. Hemodynamically, the pressure in the aortic sinuses is maximal during diastole, and during systole it is disproportionately decreased by Venturi effect. s
RUPTURED ANEURYSM OF AORne SINUS 595
However, both a coronary artery and a coronary A-V fistula must traverse the myocardium and the factor of myocardial relaxation, which plays an important role in augmenting coronary blood How during diastole, is present. The myocardial relaxation factor, however, is not present in the ruptured aneurysm of the aortic sinus of Valsalva into the right heart. However, if the aneurysmal opening is within the right ventricle, a mechanism similar to the myocardial relaxation factor might be a result of the decrease in intraventricular pressure during diastole. In hemodynamics, the analogy to a coronary artery and a coronary A-V fistula is applied to a ruptured aneurysm of the aortic sinus of Valsalva into the right ventricle.t-" Therefore, in the ruptured aneurysm of the aortic sinus of Valsalva into the right ventricle, the pressure gradient between the opening of the right ventricle and aortic sinuses is maximal during diastole and minimal during systole. Under these circumstances, maximal How of left-to-right shunt through the opening would be during diastole and contributed to diastolic accentuation of continuous murmur. This accentuation correlated with the cineangiogram which demonstrated that most of the flow was in diastole." This case showed only a diastolic murmur without aortic regurgitation. In this case, since the opening was small without a ventricular septal defect and was through the myocardium of the ventricular septum, during systole the opening might be constricted and presumably closed with myocardial contraction. The pressure gradient between the aortic sinuses and right ventricle might disappear in systole and the left-to-right shunt did not occur during systole through opening. Therefore, the blood flow through the opening was only during diastole and contributed only to a diastolic murmur. Furthermore, in this case, ventricular septal defect and aneurysmal obstruction of right ventricular outflow tract, which lead to systolic murmur, were not seen.2,6,~ Thus, this patient demonstrated only a diastolic murmur without aortic regurgitation. REFERENCES
1 Evans JW, Harris TR, Brody DA: Ruptured aortic aneurysm. Case report with view of clinical features. Am Heart J 61:408, 1961 2 Segal BL, Likoff W, Novack P: Rupture of sinus of Valsalva aneurysm. Am J CardioI12:544, 1963 3 Lin TK, Crockett JE, Dimond EG: Ruptured congenital aneurysm of the sinus of VaIsalva. Am Heart J 51:446, 1956 4 Lippshutz EJ, Wood LW: Rupture of an aneurysm of the sinus of Valsalva. Am J Med 28:859, 1960 5 Hong PL, Lee SS, Kim SW, et al: Unusual manifestations of ruptured aneurysm of the aortic sinus. J Thorac Cardiavase Surg 51:507, 1966 6 Oram S, East T: Rupture of aneurysm of aortic sinus of Valsalva into the right side of the heart. Br Heart J 17:541, 1955 7 Sakakibara S, Konno S: Congenital aneurysm of sinus of Valsalva. Am Heart J 63:708, 1962 8 Wiggers CJ: Physiology in Health and Disease (ed 5).
588 GREENBERG ET AL
Philadelphia, Lea and Febiger, 1949, quoted in Am Heart
J 61:414, 1961
9 Morgan JR, Rogers AK, Fosburg RG: Ruptured aneurysm of the sinus of Valsalva. Chest 61:640, 1972
Acute Respiratory Failure following Severe Arsenic Poisoning* Charles Greenberg, M.D.; Scott Davies, M.D.; Thomas McGowan, M.D.; Anna Scharer, M.D.; and Charles Drage, M.D.
A 47-year-old man had an episode of severe respiratory failure after acute intoxication with arsenic. Features of the initial cUnicai presentation included nausea, vomiting, and diarrhea, acote psychosis, dUluse skin rash, and marked pancytopenia. A peripheral neuropathy then developed which resulted in severe weakness of all muscles of the Umbs, the shoulder and pelvic girdles, and the trunk. The neuropathy continued to progress despite treatment with dimercaprol (BAL in oil). Five weeks after the initial exposure, the patient was no longer able to maintain adequate ventilation and required mechanical ventilatory support. Improvement in the patient'. neuromuscular status permitted successful weaning froID the ventilator after one month of mechanical ventilation. Long-term foUow-up revealed no further respiratory difficulty and slow improvement in the strength of the peripheral muscles.
he clinical features of arsenic poisoning have been well described and include a peripheral neuropathy which may be severe. 1 Although respiratory failure may complicate a wide range of neuropathic processes, including the Guillain-Barre syndrome, poliomyelitis, and acute intermittent porphyria, there are no detailed reports of respiratory failure as a sequel of acute arsenic intoxication. We report a case of respiratory failure due to extreme weakness of the respiratory muscles in a patient who survived an acute intoxication with arsenic. The report details the time course of this complication of arsenic poisoning and documents the eventual reversibility of the respiratory failure. CASE REPoRTS
A 47-year-old farmer was admitted to a local hospital with nausea, vomiting, and diarrhea. During the fourth hospital day, mental changes consisting of delusions and hallucinations developed, and the patient was referred to the Minneapolis Veterans Administration Medical Center. The patient, at the time of transfer, was unable to give any coherent history. An interview with the patient's wife established that he was a farmer and had exposure to several kinds of insecticides. He used no drugs and was not a heavy drinker of alcohol. ·From the Deparbnent of Internal Medicine, University of Minnesota School of Medicine, and the Medical Service, Veterans Administration Hospital, Minneapolis. Reprint requests: Dr. Schorer, VA Medical Center, Minneapolis 55417
CHEST, 76: 5, NOVEMBER, 1979