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BACKGROUND: Autopsy studies reveal that left ventricular free wall rupture (LVFWR) accounts for 7% to 24% of deaths after myocardial infarction. The condition occurs up to 10 times more often than papillary muscle or interventricular septal rupture. A high index of suspicion must be maintained to differentiate LVFWR from infarct extension, cardiogenic shock, pulmonary embolus, and even Dressler's syndrome. METHODS: Since 1980, we have operated on 18 patients with LVFWR. Fourteen patients had experienced "blow-out" rupture associated with cardiogenic shock. Four patients had "stuttering" ruptures, a less spectacular occurrence. Echocardiography was the most important diagnostic tool. Repair was performed, usually using infarctectomy and direct suture closure. RESULTS: Eleven patients (61%) died after operation, 4 patients as a result of rerupture 1 to 12 hours after operation. Recently, we have used a "patch/glue" technique to repair ruptures in 2 patients. We believe this technique is superior to direct suture closure in preventing rerupture. There have been 7 long-term survivors (39%) from 6 months to 15 years. CONCLUSIONS: Left ventricular free wall rupture is not always sudden and dramatic. Yet, the operating staff must be willing to race to the operating room even with the patient in full resuscitation. Echocardiography is the most sensitive and efficient diagnostic tool. All rupture sites should be aggressively repaired, possibly combining direct suture and patch/glue techniques.

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Blowout rupture of the myocardium is intended to describe a syndrome of sudden hemodynamic deterioration after myocardial infarction. Characterized by abrupt hypotension, cardiac tamponade, or electromechanical dissociation, it is an emergency of the first order with no time for cardiac catheterization. Frequently one must make the diagnosis and race for the operating room almost simultaneously. We have managed four such patients, one with a ruptured false aneurysm and three patients with acute rupture of recently infarcted myocardium. All patients were placed on femoro-femoral bypass initially and all survived operation. Two patients died in the hospital of irreversible brain damage and two are long-term survivors. A high index of suspicion, a well-coordinated operating team, and a willingness to take the bold step to the operating room, frequently on the basis of clinical judgment alone, are necessary to salvage patients with this syndrome.

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A modified micro solid-phase radioimmunoassay (RIA) for antibody to hepatitis A virus (anti-HAV) was developed. This double antibody procedure was performed by coating the surface of a polyvinyl microtiter plate "well" with 200 microliter of a 1:1,000 dilution of a patient's test serum. Purified HAV and 125I-labeled immunoglobulin G (IgG) anti-HAV were then sequentially added to form an antibody sandwich. The specificity and sensitivity of the RIA procedure for anti-HAV were verified by examination of coded human and chimpanzee serum specimens. Radioimmunoassay of early-acute-phase serum specimens from human cases of hepatitis A revealed the presence of anti-HAV activity. Differential examination by RIA of IgG and IgM fractions of acute-phase sera from experimentally infected chimpanzees demonstrated that IgM contained the bulk of the anti-HAV activity. A modification of the RIA procedure for anti-HAV (RIA-IgM blocking), incorporating an incubation step with anti-IgM (Mu chain specific), was further shown to differentiate acute- from convalescent-phase hepatitis A sera. This adapted RIA-IgM blocking procedure required less than 1 microliter of a single acute-phase serum specimen for the diagnosis of viral hepatitis A.

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The cities of Portland, Oregon, and Buffalo, New York, each experienced a restaurant-associated foodborne outbreak of viral hepatitis type A during 1975. Although there were several food handlers ill with viral hepatitis A in each of the restaurants involved, each outbreak was the apparent result of food contamination by a single food handler. In the Buffalo outbreak, food contamination was documented to have occurred for a brief period of time six days prior to onset of any symptoms in the index case. These outbreaks point out the uncommon occurrence of food contamination by individuals ill with type A viral hepatitis, the usefulness of two types of food questionnaires in identifying the vehicle(s) of transmission, and the apparent lack of benefit of widespread immune serum globulin administration as a control measure in this setting.

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The occurrence of a common source hepatitis A epidemic among the residents of a New England state mental institution where hepatitis B is hyperendemic provided an opportunity to observe concurrent infections with both agents. Nine HBsAg-positive individuals developed hepatitis A infections documented by hepatitis A antibody seroconversion in eight. The incidence of hepatitis A infections in susceptible HBsAg-positive persons (67%) did not differ from that in HBsAg-negative individuals (63%). The icteric to anicteric infection ratio in the HBsAG-positives (1:1.7) was similar to that in the negatives (1:2.1), and the clinical course in the antigen positives did not differ significantly from that of the antigen negatives. In addition to confirming previous reports that the viruses of hepatitis A and B are immunologically distinct, these results document that infection with either is independent of the other, and that the morbidity from simultaneous infection is no greater than that caused by either alone.

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In a 2-month period four cases of hepatitis B occurred in hospital staff. Three months later two patients, hospitalized for open-heart surgery when the staff members had been infected, developed acute hepatitis B. Sera from all six ill individuals were subtype ayw and e-determinant positive. Epidemiologic investigation showed that the four staff had been exposed 3 months earlier to an asymptomatic hepatitis B surface antigen-positive (HBsAg) patient who was also e positive. To determine transmission from staff to patients study of 17 open-heart surgery patients was undertaken. Four of 17 were either HBsAg or anti-HBs positive. No correlation between infection and contact with three of four ill staff members or receipt of blood products was noted; however, 22 (46%) of 48 arterial blood gas specimens had been obtained from infected patients by one staff member, an inhalation therapist; this compared with seven (4%) of 157 specimens she obtained from control subjects (P less than 0.001). Furthermore, she handled indwelling arterial cannulae 25 (76%) of 33 times in infected patients compared with three (3%) of 95 times in control subjects (P less than 0.001). Transmission may have occurred via the arterial cannulae from a severe exudative dermatitis on the therapist's hands.

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Sera of 103 carriers of hepatitis B surface antigen were assayed for e-antigen and anti-e. Twenty-four were e-antigen-positive, 31 anti-e-positive, and 48 had neither detectable (e-negative). Aminotransferases were elevated in 75% of the e-antigen-positive carriers compared with 25% of e-negative carriers (P less than 0.001) and 13% of anti-e-positive carriers (P less than 0.001). Serum DNA polymerase activity was significantly higher in the e-antigen-positive carriers than in carriers without e-antigen. Dane particles were shown in 10 of 12 carriers with e-antigen, compared with one of 12 e-negative carriers (P less than 0.0003) and none of 12 anti-e-positive carriers (P less than 0.00003). These results suggest that ongoing hepatitis B viral replication is more active in e-antigen-positive carriers than in carriers without e-antigen, a finding that may help explain the high prevalence of chronic active hepatitis described in these individuals.

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Between July 24 and Aug. 19, 1974, an outbreak of pyrogenic reactions occurred in patients at a private haemodialysis centre in a suburb of Washington, D.C. 49 reactions characterised by chills, fever, and hypotension occurred in twenty-three of the seventy patients dialysed during this period. No infections could be documented in any of the affected individuals. Despite the fact that only low levels of gram-negative bacterial contamination of the haemodialysis system were found, high levels of endotoxin contamination of dialysis fluid and endotoxaemia in patients experiencing overt reactions were recorded using the Limulus lysate test. The cause of these reactions was traced to an increase in endotoxin contamination of the tap water used to prepare dialysate, possibly caused by an increase in the algae levels in the local water source. The installation of a reverse osmosis system for water treatment may be a solution to the problem of endotoxin contamination of water used to prepare dialysis fluid.

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Gram-negative bacteria can multiply relatively fast in a variety of hospital associated fluids ranging from distilled, deionized, reverse osmosis, and softened water, which are normally considered devoid of nutrients, to intravenous solutions and fluids associated with hemodialysis. Excessive levels of these bacteria in the dialysate of artificial kidney machines can be responsible for pyrogenic reactions or sepsis or both.

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