This study was conducted to identify patients at high risk of the development of Pulmonary Embolism (PE) after open heart surgery, to evaluate pertinent diagnostic methods, and to assess the mortality associated with this complication. We evaluated the records of 2,551 consecutive patients who underwent open heart surgery over a 10-year period to identify those patients in whom PE developed. All surgical reports, ventilation/perfusion scans, pulmonary angiograms, and autopsies from the same period were also reviewed. Preoperative and postoperative risk factors for pulmonary embolism were also analyzed, as well as the outcome of this complication in each type of surgical procedure. Pulmonary embolism was identified in 69 (2.7%) patients after open heart surgery, in 43 (62.3%) of whom the diagnosis was established within the first week of surgery. Factors associated with high incidence for PE were hyperlipidemia, congestive heart failure and heparin-induced thrombocytopenia (P < 0.001); obesity and prolonged mechanical ventilation (P < 0.005); and prior right heart catheterization by the femoral approach and prior PE and/or deep vein thrombosis (P < 0.05). The diagnosis of PE was established by a high-probability ventilation/perfusion scan in 25 patients, by pulmonary angiography in 42 (29 of whom had prior V/Q scan read as intermediate or low probability for PE) and by autopsy in two patients. The mortality rate in patients who had PE was 7.2%, while in those without this complication it was 3.2%. These findings suggest that aggressive approach for the diagnosis of PE by pulmonary angiography whenever the V/Q scan is not read as high probability is crucial in patients with recent open heart surgery; such approach may identify patients with PE at an early stage and may have an impact in reducing mortality incurred by this complication. This diagnostic assessment should be emphasized in the perioperative period, especially in patients with multiple significant and identifiable risk factors for PE.
Cardiac rupture complicating acute myocardial infarction (AMI) remains a serious diagnostic and therapeutic challenge. The authors present 27 consecutive patients who died from cardiac rupture following AMI. These included 22 patients from 1975 through 1983 (prethrombolytic era) and 5 patients from 1984 through 1992 (postthrombolytic era) and all had postmortem examination. There were 16 men and 11 women with a mean age of seventy-two years. Myocardial infarction was anterior/anterolateral in 10 and inferior/inferoposterior in 17. Cardiac rupture followed AMI within one day in 14 (52%), two to five days in 8 (30%), and six to fourteen days in 5 (18%). Chest pain followed by sudden hypotension leading to electromechanical dissociation was the common terminal event. Cardiopulmonary resuscitation was unsuccessful in all patients. Postmortem findings showed three-vessel coronary disease in 21 (78%) and two-vessel disease in 6 (22%). Isolated free left ventricular wall rupture was found in 22 (81%), was anterior/anterolateral in 13 (48%), posterior in 9 (33%), and in conjunction with interventricular septum or papillary muscle in 5 (18%). Patients encountered in this series were mostly elderly hypertensives with multivessel coronary disease and postinfarction angina. Furthermore, cardiac rupture commonly occurred within the first five days of AMI and cardiopulmonary resuscitation was uniformly unsuccessful. During the thrombolytic era at their institution, this complication is now being seen much less often. These observations suggest that such interventions are expected to have a favorable impact on reducing the incidence of this catastrophic event.
The appearance of acute iatrogenic dissection of the coronary arteries during coronary angiography is described in five patients. Specific signs of dissection include: 1) initimal flap, 2) delayed flow, 3) loss of side branches, 4) periostial contrast "puddling," and 5) unusually small size coronary artery with atypical smooth walls. Recognition of the radiographic patterns of this complication should permit distinction from coronary spasm, thrombosis, and embolization. Recent advent of alternate forms of therapy (streptokinase infusion, angioplasty) makes it imperative to precisely diagnose the dissection to avoid possible catastrophic results.
Two patients with biopsy-proven amyloid restrictive cardiomyopathy were presented. Both cases showed ventricularization of an elevated right atrial pressure wave form in absence of tricuspid regurgitation. Possible explanations for this finding as well as its clinical implications are discussed. This observation indicates that ventricularization of right atrial pressure wave form could be a useful hemodynamic sign in amyloid restrictive cardiomyopathy in absence of tricuspid regurgitation. Furthermore, such a finding does not seem to be specific for tricuspid regurgitation.
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