Herediter anjioödem hastalarında atak anında ve atak dışı dönemde pulmoner arteriyel stıffness değerlendirilmesi
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Tarih
2024
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Necmettin Erbakan Üniversitesi, Tıp Fakültesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Amaç: Herediter anjioödem, bradikinin ilişkili anjioödem atakları ile seyreden, tedavi edilmediği
taktirde hayati tehlike oluşturan bir hastalıktır. Bu çalışmamızda herediter anjioödem
hastalarında ekokardiyagrafik yöntemle atak döneminde ve atak dışı dönemde pulmoner arteriyel
stiffness değerlendirilmesi yapılarak; kardiyovasküler hastalık gelişimi, pulmoner hipertansiyon
gelişiminin erken tespiti, kardiyovasküler mortalite ile ilişkisi hakkında yorum yapmak ayrıca
güncel pratiğe pulmoner arteriyel stiffness ölçümünün atak tanı kriteri olarak kullanılabilirliği
yönünden değerlendirilmesi amaçlanmıştır.
Yöntem: Çalışmaya Necmettin Erbakan Üniversitesi Meram Tıp Fakültesi Erişkin İmmünoloji
ve Alerji Hastalıkları polikliniğine atak ve atak dışı dönemde başvuran toplamda 34 Herediter
anjioödem hastası ve sağlıklı gönüllülerden oluşan 20 kontrol grubu dahil edilmiştir.
Hipertansiyon, koroner arter hastalığı, hipertirodi tanısı olan hastalar çalışma dışı bırakıldı. Hasta
ve kontrol grubunun sistolik ve diyastolik fonksiyonları, IVRT, IVCT, ET, pulmoner arteriyel
stiffness hesaplanması için pulmoner akışın maksimum frekans kayması(MSS) ve akselerasyon
zamanı (PAAT) ölçülmüştür. PAS hesaplanması için; PAS=MSS/PAAT formülü kullanılmıştır.
Miyokardiyal performans indeksi IVRT+IVCT/ET formülünden hesaplanmıştır.
Bulgular: Çalışmaya 34(63.0%) herediter anjioödem hastası, 20(37.0%) kontrol grubu
olmak üzere toplam 54 hasta dahil edilmiştir. Herediter anjioödem tanısı olan hastaların
22(64.7%) si kadın, 12(35.3%) ü erkektir. Kontrol grubundaki hastaların 10(50.0%) u kadın,
10(50.0%) erkektir. Hastaların yaş ortalaması 38.03∓11.57 yıl, kontrol grubunun yaş ortalaması
37.60∓11.74 yıldır. Yaş ve cinsiyetin gruplara dağılımı homojendir. Hasta ve kontrol grubunun
eko parametreleri arasındaki istatistiki karşılaştırmada LVESD (p=0.027), SEPTAL E (p=0.033),
SEPTAL A (p=0.043), IVCT (p=0.038), MPI (p=0.007) değerleri hasta grubunda kontrol
grubuna göre yüksek bulunmuştur ve istatistiki olarak anlamlıdır. LAVİ(ml) değeri hasta
grubunda kontrol grubundan düşük bulunmuştur, ve istatistiki olarak anlamlıdır(p=0.042). PAS
değeri ve diğer ekokardiyografik değişkenler herediter anjioödem hastaları ile kontrol grubu
hastaları arasındaki farklılıklar istatistiki olarak anlamlı değildir (p>0.05). Herediter anjioödem
hastalarnın yaş, atak sıklığı, hastalık süresi ve tanıda gecikme süreleri ile LVESD; SEPTAL E,
SEPTAL A, IVCT, MPI değerleri arasında anlamlı ilişki saptanmamıştır(p>0.005). Herediter
anjioödem hastalarının atak dışı ve atak verileri arasındaki farklılıklar istatistiki olarak anlamlı
değildir (p>0.05).
Sonuç: Çalışmamızda pulmoner arteriyel stiffness değerlendirilmesi hasta ve kontrol grubu
arasında ayrıca hasta grubunda atak ve atak dışı dönem karşılaştırıldığında istatistiki anlamlı bir
fark bulunmamış olup daha büyük hasta gruplarında PAS değerlendirilmesine ihtiyaç vardır. MPI
hasta grubunda kontrol grubuna yüksek bulunmuş olup herediter anjioödem hasta grubunda
gelişecek kardiyovasküler hastalıkların habercisi olabilir. Herediter anjioödem hasta grubunda
takipte kardivak etkiler açısından MPI kullanılabilir. Önceki çalışmalarla birlikte
değerlendirildiğinde herediter anjioödem hastalarında kardiyovasküler hastalık riski artmıştır,
düzenli kardiyovasküler sistem takibi önerilir.
Objective: Hereditary angioedema is a life-threatening disease characterized by bradykininassociated angioedema attacks. In this study, we aimed to evaluate pulmonary arterial stiffness in patients with hereditary angioedema by echocardiagraphic method during the attack and nonattack periods; to comment on the development of cardiovascular disease, early detection of pulmonary hypertension, its relationship with cardiovascular mortality and to evaluate the use of pulmonary arterial stiffness measurement as an attack diagnostic criterion in current practice. Method: A total of 34 patients with hereditary angioedema who presented to Necmettin Erbakan University Meram Medical Faculty Adult Immunology and Allergy Diseases outpatient clinic during attack and non-attack periods and 20 controls consisting of healthy volunteers were included in the study. Patients with hypertension, coronary artery disease and hyperthyroidism were excluded from the study. Systolic and diastolic functions, IVRT, IVCT, ET were evaluated in the patient and control groups. Maximum frequency shift (MSS) and acceleration time (PAAT) of pulmonary flow were measured to calculate pulmonary arterial stiffness. The formula PAS=MSS/PAAT was used to calculate PAS. Myocardial performance index was calculated from the formula IVRT+IVCT/ET. Results: A total of 54 patients including 34(63.0%) hereditary angioedema patients and 20(37.0%) control group were included in the study. Among the patients with hereditary angioedema, 22(64.7%) were female and 12(35.3%) were male. In the control group, 10(50.0%) were female and 10(50.0%) were male. The mean age of the patients was 38.03∓11.57 years and the mean age of the control group was 37.60∓11.74 years. The distribution of age and gender in the groups was homogeneous. In the statistical comparison between the echo parameters of the patient and control groups, LVESD (p=0.027), SEPTAL E (p=0.033), SEPTAL A (p=0.043), IVCT (p=0.038), MPI (p=0.007) values were higher in the patient group compared to the control group and were statistically significant. La volume (ml) value was lower in the patient group than in the control group, and statistically significant (p=0.042). The differences in PAS value and other echocardiographic variables between patients with hereditary angioedema and control group patients were not statistically significant (p>0.05). No significant correlation was found between age, frequency of attacks, duration of disease and delay in diagnosis and LVESD; SEPTAL E, SEPTAL A, IVCT, MPI values of hereditary angioedema patients (p>0.005). Differences between non-attack and attack data of hereditary angioedema patients were not statistically significant (p>0.05). Conclusion: In our study, no statistically significant difference was found in the evaluation of pulmonary arterial stiffness between the patient and the control group and also when the attack and non-attack periods were compared in the patient group, and PAS evaluation is needed in larger patient groups. MPI was found to be higher in the patient group compared to the control group and may be a harbinger of cardiovascular diseases that will develop in the hereditary angioedema patient group. MPI may be used in the hereditary angioedema patient group in terms of cardivac effects in follow-up. When evaluated together with previous studies, the risk of cardiovascular disease is increased in patients with hereditary angioedema and regular cardiovascular system follow-up is recommended.
Objective: Hereditary angioedema is a life-threatening disease characterized by bradykininassociated angioedema attacks. In this study, we aimed to evaluate pulmonary arterial stiffness in patients with hereditary angioedema by echocardiagraphic method during the attack and nonattack periods; to comment on the development of cardiovascular disease, early detection of pulmonary hypertension, its relationship with cardiovascular mortality and to evaluate the use of pulmonary arterial stiffness measurement as an attack diagnostic criterion in current practice. Method: A total of 34 patients with hereditary angioedema who presented to Necmettin Erbakan University Meram Medical Faculty Adult Immunology and Allergy Diseases outpatient clinic during attack and non-attack periods and 20 controls consisting of healthy volunteers were included in the study. Patients with hypertension, coronary artery disease and hyperthyroidism were excluded from the study. Systolic and diastolic functions, IVRT, IVCT, ET were evaluated in the patient and control groups. Maximum frequency shift (MSS) and acceleration time (PAAT) of pulmonary flow were measured to calculate pulmonary arterial stiffness. The formula PAS=MSS/PAAT was used to calculate PAS. Myocardial performance index was calculated from the formula IVRT+IVCT/ET. Results: A total of 54 patients including 34(63.0%) hereditary angioedema patients and 20(37.0%) control group were included in the study. Among the patients with hereditary angioedema, 22(64.7%) were female and 12(35.3%) were male. In the control group, 10(50.0%) were female and 10(50.0%) were male. The mean age of the patients was 38.03∓11.57 years and the mean age of the control group was 37.60∓11.74 years. The distribution of age and gender in the groups was homogeneous. In the statistical comparison between the echo parameters of the patient and control groups, LVESD (p=0.027), SEPTAL E (p=0.033), SEPTAL A (p=0.043), IVCT (p=0.038), MPI (p=0.007) values were higher in the patient group compared to the control group and were statistically significant. La volume (ml) value was lower in the patient group than in the control group, and statistically significant (p=0.042). The differences in PAS value and other echocardiographic variables between patients with hereditary angioedema and control group patients were not statistically significant (p>0.05). No significant correlation was found between age, frequency of attacks, duration of disease and delay in diagnosis and LVESD; SEPTAL E, SEPTAL A, IVCT, MPI values of hereditary angioedema patients (p>0.005). Differences between non-attack and attack data of hereditary angioedema patients were not statistically significant (p>0.05). Conclusion: In our study, no statistically significant difference was found in the evaluation of pulmonary arterial stiffness between the patient and the control group and also when the attack and non-attack periods were compared in the patient group, and PAS evaluation is needed in larger patient groups. MPI was found to be higher in the patient group compared to the control group and may be a harbinger of cardiovascular diseases that will develop in the hereditary angioedema patient group. MPI may be used in the hereditary angioedema patient group in terms of cardivac effects in follow-up. When evaluated together with previous studies, the risk of cardiovascular disease is increased in patients with hereditary angioedema and regular cardiovascular system follow-up is recommended.
Açıklama
Anahtar Kelimeler
Herediter anjioödem, Hereditary angioedema, pulmoner arteriyel stiffness, pulmonary arterial stiffness, miyokardiyal performans indeksi, myocardial performance index
Kaynak
WoS Q Değeri
Scopus Q Değeri
Cilt
Sayı
Künye
Büyükboz, E. (2024). Herediter anjioödem hastalarında atak anında ve atak dışı dönemde pulmoner arteriyel stıffness değerlendirilmesi. (Yayınlanmamış tıpta uzmanlık tezi) Necmettin Erbakan Üniversitesi, Tıp Fakültesi Dahili Tıp Bilimleri Bölümü İç Hastalıkları Anabilim Dalı, Konya.
