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Abstract ACEI are being used increasingly in the treatment of hypertension and heart failure, as asthma and hypertension may coexist, so the importance of ACEI to asthma excacerbation is potentially important. This is a prospective study that examined the effect of ACEI on airway responsiveness and this study was conducted on eighty newly diagnosed hypertensive patients and ten healthy subjects. They were classified into 3 groups. Group (I) : Including 40 hypertensive patients receivmg ACEI, it was subdivided into : group Ia: Included (10) hypertensive asthmatic patients receiving short acting ACEI (captopril). group Ib: Included (10) hypertensive non asthmatic patients receiving the same short acting (ACEI). group Ic : Include (10) hypertensive asthmatic patients receiving long acting (ACE!) Ramipril. Q 146;p . Included (10) hypertensive non asthmatic patients receiving long acting”ACEI Ramipril. Group II: Included 40 hypertensive patients receiving other antihypertensive drugs, It will be subdivided into : group II a: Included (10) hypertensive asthmatic patients receiving calcium channel blocker (Nifedipine). group II b: Included (10) hypertensive non asthmatic patients receiving calcium channel blocker (Nifedipine). group Il c: Inlcuded (10) hypertensive asthmatic patients receiving diuretics (frusemide ). group II d: Included (10) hypertensive non asthmatic receiving beta blocker (Atenolol). Group III : Included (10) healthy subjects served as a control group. To all subjects ventilatory functions and provocation studies were done among other routine investigation. - This study revealed : 1-Two cases among 10 hypertensive non asthmatic patients who received captopril (20%) showed bronchial hyperreactivity with reduction of their PD20 to less than 3130Jlg methacholine after 72 h (\~dtwo weeks of captopril. 2-One case among 10 hypertensive asthmatic patients (10%) who received short acting ACEI (captopril) showed deterioration of his asthma symptoms with reduction of his PD20 to less than 130Jlg methacholine two weeks after captopril. 3-0ne case out of 10 (10%) hypertensive non asthmatic who received Ramipril (long acting ACEI) showed bronchial hyperreactivity two weeks after Ramipril therapy. ;,r 4-0ne case out of 10 hypertensive asthmatic subject (100/0)who received Ramipril showed deterioration of his asthma symptoms and reduction of his PD20 to less than 300llg methacholine two weeks after Ramipril therapy. 5-Non of the patient in group (II) who received other antihypertensive drugs (Nifedipine frusemide- Atenolol) showed bronchial hyperreactivity or chanage in his PD20 . • Two cases out of nine cases to whome echocardiogrpahy was done showed early subclinical left ventricular dysfunction with no effect on their PD20 or ventilatory function. • from this study it was concluded that. • ACEI can cause cough in 10-20% of hypertensive asthmatic and hypertensive non asthmatic patients. • Study of bradykinin level in (BAL) of patients who developed cough after the use of (ACEI) may be the aim of a further study for explanation of cough induced by this class of drugs• Hypertension may cause subclinical left ventricular dysfunction /;. manifested by EfA ratio less than 0.86 (Table 23). So hypertensive patient must be examined by echo cardiography regularly . • Asthmatic hypertensive patients must stope ACEI treatment when he developed” dry cough. • Study of bradykinin level in (BAL) of patients who developed cough after the use of ACEI may be useful for explanation of cough associated with these drugs. • Hypertensive patient may be examined by echo cardio.graphy for the diagnosis of subclinical left ventricular dysfunction. |