ABSTRACT
We present a case of cardiogenic shock due to acute thrombotic occlusion of the left main coronary artery in Kawasaki's aneurysmal coronary artery disease. The patient was treated with PTCA as a bridge to CABG. Because of a persistent low-output syndrome, orthotopic heart transplantation was successfully performed three days later. The patient is alive and well one year after the event.
Subject(s)
Coronary Disease/diagnosis , Mucocutaneous Lymph Node Syndrome/complications , Acute Disease , Adult , Angioplasty, Balloon, Coronary , Cardiac Output, Low/etiology , Cardiac Output, Low/surgery , Combined Modality Therapy , Coronary Artery Bypass , Coronary Disease/complications , Coronary Disease/pathology , Coronary Disease/therapy , Coronary Vessels/pathology , Electrocardiography , Female , Heart Transplantation , Humans , Postoperative Complications/etiology , Postoperative Complications/surgerySubject(s)
Angioplasty, Balloon, Coronary , Myocardial Ischemia/therapy , Stents , Aged , Angina Pectoris/diagnosis , Angina Pectoris/therapy , Angina, Unstable/therapy , Coronary Angiography , Follow-Up Studies , Humans , Middle Aged , Myocardial Infarction/therapy , Myocardial Ischemia/diagnosis , Randomized Controlled Trials as Topic , Recurrence , Risk Factors , Time FactorsABSTRACT
OBJECTIVES: This study investigated the value of sestamibi scintigraphy in assessing residual ischemia after anterior myocardial infarction. BACKGROUND: Serial imaging with sestamibi, the uptake and retention of which correlate with regional myocardial blood flow and viability, has been used to estimate salvaged myocardium and risk area after acute infarction. We recently documented that recovery of perfusion and contraction in the infarcted area may continue well after the subacute phase, suggesting myocardial hibernation. Some underestimation of viability in the setting of hibernating myocardium by sestamibi imaging has been reported. METHODS: We studied 58 patients in stable condition after Q wave anterior infarction. Regional perfusion and function were quantitatively assessed by sestamibi tomography and two-dimensional echocardiography at 4 to 6 weeks and at 7 months after infarction. In sestamibi polar maps, abnormal areas with tracer uptake > 2.5 SD below our reference values were computed at rest and after symptom-limited exercise. On two-dimensional echocardiography the ejection fraction and extent of rest wall motion abnormalities were assessed by a computerized system. All patients had coronary angiography between the two studies. RESULTS: At 7 months the extent of rest sestamibi defect was significantly reduced in 40 patients (69%, group 1) and unchanged in 18 (31%, group 2). Rest wall motion abnormalities and ventricular ejection fraction significantly improved in group 1 but not in group 2. Underlying coronary disease, patency of the infarct-related vessel and rest sestamibi defect extent at 5 weeks were comparable between the two groups. At 7 months, an increase in the reversible (stress-rest defect) tracer defect was observed in group 1 (p < 0.05) despite a smaller stress-induced hypoperfusion (p < 0.05). Reversible sestamibi defects and stress hypoperfusion were unchanged in group 2. In 38 (95%) of 40 group 1 patients, the area showing reversible sestamibi defects at 7 months matched the area showing fixed hypoperfusion at 5 weeks. CONCLUSIONS: The reduction in the rest tracer uptake defect that can occur late after infarction may affect the assessment of ischemic burden by sestamibi imaging early after anterior myocardial infarction.
Subject(s)
Heart/diagnostic imaging , Myocardial Infarction/diagnostic imaging , Myocardial Ischemia/diagnostic imaging , Technetium Tc 99m Sestamibi , Adult , Cohort Studies , Echocardiography , Humans , Male , Middle Aged , Prospective Studies , Radionuclide ImagingABSTRACT
Myocardial sestamibi uptake reflects regional flow distribution and cellular integrity; however, some segments showing reduced tracer uptake at rest may consist of viable, although hypoperfused, myocardium. It is speculated that the administration of nitroglycerin (NTG) before the sestamibi injection would improve the tracer uptake in resting hypoperfused regions. Thirty-six stable patients with previous myocardial infarction (56 +/- 2 years; mean ejection fraction 42 +/- 2%), in whom perfusion defects could be seen at resting sestamibi tomography, repeated the scintigraphic study 2 to 6 days later, receiving NTG (0.3 to 0.6 mg sublingually) before the tracer injection. The size of the tracer uptake defect was quantified from circumferential profiles in 3 short-axis slices by integrating the area below the lower normal limit (mean -2 SD). After NTG, the mean perfusion defect significantly decreased (from 6,324 +/- 619 to 5,365 +/- 516, p < 0.01). The defect was reduced beyond the reproducibility limits in 20 patients (56%, group 1) and was unchanged or increased in 16 (44%, group 2). The resting sestamibi defect size was comparable between the 2 groups. The average percent reduction of the perfusion defect after NTG was 29 +/- 4% (range 7 to 74).(ABSTRACT TRUNCATED AT 250 WORDS)
