Farkedilmeden geçirilmiş miyokard infarktüsünün klinik özellikleri ve miyokard perfüzyon sintigrafisi bulguları
Küçük Resim Yok
Tarih
2003
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Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Amaç: Çalışmamızda fark edilmeden (FGMİ) ve farkında olunarak geçirilmiş Mİ (FOMİ)'lerin klinik, demografik ve miyokard perfüzyon sintigrafik (MPS) özelliklerini karşılaştırarak ve Mİ'nin sessiz geçirilmesiyle ilişkili olması muhtemel faktörleri araştırdık. Gereç ve Yöntem: MPS'de sabit defekt saptanan 73 hasta öykülerine göre FGMİ (n=29, K/E: 5/24, yaş:57±11) ve FOMİ (n=44, %60, K/E:6/38, yaş:56±10) olarak 2 gruba ayrıldı. Hastalara egzersiz testi öncesi 8mCi ve egzersiz testinde (Bruce protokolüyle) doruk egzersizde 25 mCi Tc99m-sestamibi enjekte edilerek test öncesi ve sonrası görüntüler alındı. Bulgular: Çalışmamızda MPS ile saptanan FGMİ sayısı EKG'ye oranla anlamlı olarak yüksekti (29/73=%40'a 22/73=%30, p<0.05). FOMİ'ye kıyasla FGMİ'de DM sıklığı artmış, preinfarktüs angina (PİA) ve ailede koroner arter hastalığı varlığı (AKAH) azalmış olarak saptandı (sırasıyla p<0.03, p<0.05, p<0.03). FGMİ'de infarkt boyutu küçük olan hasta sayısı FOMİ'ye göre daha fazla (p<0.05), geniş Mİ alanına sahip hasta sayısı ise daha az bulundu (p<0.03). FOMİ grubunda FGMİ'ye kıyasla anterior, septum ve apikal bölge tutulumları anlamlı olarak yüksek saptandı (sırasıyla p<0.05, p<0.05, p<0.04). Korelasyon analizinde FGMİ' ile PİA ve AKAH arasında negatif (r=-0.32, p<0.05, r=-0.37, p<0.04), DM varlığı ile pozitif bir ilişki saptandı (r=0.35, p<0.05). Sonuç: Bu sonuçlar DM varlığı, PİA ve AKAH yokluğunun FGMİ için bir risk faktörü olduğunu düşündürmüştür. FGMİ'nin tanısı MPS'de gözlenen sabit defektlerin varlığı ile güvenle konulabileceği gibi, Mİ'alanının boyut ve lokalizasyonu da daha net bir şekilde belirlenebilir.
Aim: In our study, we compared to clinic, demographic and myocardial perfusion scintigraphic (MPS) features of recognized and unrecognized myocardial infarctions and we investigated potential factors associated with experiencing silent MI. Materials and Methods: In (MPS), 73 patients having fixed defect were divided into two groups according to their medical history: UMI (n=29, F/M: 5/24, age:57±11) and RMI (n=44, F/M:6/38, age:56±10). The patients were given 8mCi, before the exercise testing (with Bruce protocoly), during the exercise testing by injecting 25mCi Tc99m-sestamibi at the peak exercise then images were recorded both before and after the test. Results: In our study, the number of UMI detected by MPS was significantly high compared to those diagnosed with ECG (22/73:30% to 29/73:40%, p<0.05). In comparison to RMI, the frequency of DM increased in UMI, the existence of family history of coronary artery disease (FHCAD) and preinfarct angina (PIA) decreased. It was found that in UMI the number of patients whose infarct dimension is small was higher than that of RMI (p<0.05), however, the number of patients who have wide MI area is the less (p<0.03). In comparison to UMI, in RMI group, region involvements of anterior, septum and apex were diagnosed significantly high (p<0.05, p<0.05, p<0.04, respectively). In correlation analysis, it was detected that there was a negative relationship between UMI and FHCAD, PIA (r=-0.32, p<0.05, r=-0.37, p<0.04, respectively), and a positive relationship UMI and the existence of DM (r=0.35, p<0.05). Conclusion: The findings suggested that the existence of DM, the absence of PIA and FHCAD as a risk to UMI. UMI can be diagnosed with the existence of fixed defects observed in MPS, besides, the location and size of MI can be pointed out much more clearly.
Aim: In our study, we compared to clinic, demographic and myocardial perfusion scintigraphic (MPS) features of recognized and unrecognized myocardial infarctions and we investigated potential factors associated with experiencing silent MI. Materials and Methods: In (MPS), 73 patients having fixed defect were divided into two groups according to their medical history: UMI (n=29, F/M: 5/24, age:57±11) and RMI (n=44, F/M:6/38, age:56±10). The patients were given 8mCi, before the exercise testing (with Bruce protocoly), during the exercise testing by injecting 25mCi Tc99m-sestamibi at the peak exercise then images were recorded both before and after the test. Results: In our study, the number of UMI detected by MPS was significantly high compared to those diagnosed with ECG (22/73:30% to 29/73:40%, p<0.05). In comparison to RMI, the frequency of DM increased in UMI, the existence of family history of coronary artery disease (FHCAD) and preinfarct angina (PIA) decreased. It was found that in UMI the number of patients whose infarct dimension is small was higher than that of RMI (p<0.05), however, the number of patients who have wide MI area is the less (p<0.03). In comparison to UMI, in RMI group, region involvements of anterior, septum and apex were diagnosed significantly high (p<0.05, p<0.05, p<0.04, respectively). In correlation analysis, it was detected that there was a negative relationship between UMI and FHCAD, PIA (r=-0.32, p<0.05, r=-0.37, p<0.04, respectively), and a positive relationship UMI and the existence of DM (r=0.35, p<0.05). Conclusion: The findings suggested that the existence of DM, the absence of PIA and FHCAD as a risk to UMI. UMI can be diagnosed with the existence of fixed defects observed in MPS, besides, the location and size of MI can be pointed out much more clearly.
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10
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5
