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Silent myocardial ischemia and the relationship with cardiovascular endorgan damage in newly found hypertensives.
AJH-APRIL 1999-VOL. 12, NO. 4, P A R T 2
POSTERS:
End Organ
j005
j006
SILENT MYOCARDIAL ISCHEMIA AND THE RELATIONSHIP WITH CARDIOVASCULAR ENDORGAN DAMAGE IN NEWLY FOUND HYPERTENSIVES. W.F. Terpstra I=, J.F. Mayn, A.J. Smit *=, P.A. de Grae~ 2, H.J.G.M. CrijnsL Academic Hospital Groningen ~ and Groningen Hypertension Service =, Groningen, The Netherlands. Hypertension is associated with increased coronary risk. This study was performed to assess the prevalence of asymptomatic ST segment depression and to determine the relationship with cardiovascular end-organ damage in newly found, eldedy hypertensives. From a population survey we included 178 new mild to moderate hypertensives (4x systolic blood pressure _>160 mmHg and/or diastolic blood pressure > 95 mmHg), aged 60 to 75 years with 53% male. Exclusion cdteria were: angina pectoris, severe atherosclerotic disease, diabetes mellitus and ST abnormalities on resting ECG. A 48 hour Holter monitor (3 channel ECG) was performed to detect episodes of ST segment depression, using the 1"1"1 rule of Cohn. Ischemic burden was calculated as number of episodes * total mm* total duration of ST segment depression. Echo left ventricular mass was calculated using the mean of 3 consecutive measurements of septum, posterior wall and end-diastolic diameter and indexed by body surface area (LVMI). Intima-media thickness (IMT) was measured in 10 prespecified segments of carotid and femoral artery. Transient ST segment depression was observed in 21 hypertensive patients, a prevalence of 12 %. In this group, a significant correlation was found between LVMI and ischemic burden (r=0.466:p=0.033). Compared to the group of hypertensives without ST segment depression, LVMI was not significantly different (111 +1-18 vs 104+/-24 g/m =, respectively). However, combined mean far wall IMT was significantly higher in hypertensives demonstrating ST segment depression (0.98+•0.21 vs 0.88+/-0,16 mm; P < 0.05). These data suggest, that vascular endorgan damage is mainly responsible for the development of silent myocardial ischemia in elderly with mild to moderate hypertension. Once myocardial ischemia has developed, an increased demand for oxygen by mass enlargement determines the seventy of myocardial ischemia.
Abnormal Baseline Endothelial Dysfunction end Thrombogenesis are related to Prognosis In Hypertemlon
Key Words:
E Edmu~ds,AD Blann, DG Beevors.GYFILip Hsemostasis Tla'ombo~s end Vascular Biology Unit, University Departmentof Medicine,City Hospital,B i m ~ England Despite high intravascular pressures, the complications of hypertension (heart attacks, sixokes) are p~edoxicully thrombotic rather than haomorrbagic. To inv¢stigatewhether baseline markers of endothelial dysfunction (von Willebrand factor, vWf), baomorheology(haematocrit, fibrinngen,plaranaviscosity),thrombogenesis(fibrin D-dirner),and platelet activation (soluble P-seleetin, sPsel) are related to outcomes, we prospectivelyfollowedup 178 patients (92 males; mean age54.52 sd14.6) with hypertension for a mean of 47.5 months (s.d 10.12). Baseline characteristicsof patients who developed cardiovascularcomplications (angina,myocardialinfarction,ccrebrovascularevents,pcnpheral vascular disease or death) (Group I) (n=24) during follow-up,were compared to thosewho remmned freeof such complications(Group H)
mean(aM.)
Group I SystolicBP nunHg 190.8(24.9) DiastolicBP nunHg 102.9(14.0) Bodymass index keCm2 27.7 (3.7) LV mass index g/m2 177.0(60.1) vWfiU/dl 130.2(31.5) Haeanateerit % 42.5 (4.4) Fibrinogeng/l 3,3 (0.6) ViscositymPa 1.73 (0.11)
Group H 187.4(28.8) 106.0(23.0) 28.5 (47) 154.7(67.2) 111.4(31.2) 42.7 (4.64) 34 ( 1.I ) 1.73 (0.29)
P value 0.57 0.39 0.40 0.17 0.017 0.91 0.61 0.35
250 (175-320) 300 (196-473)
0.018
median (IQR) D-dimerng/ml P-sclectinng/ml
305 (230-500) 260 (165-803)
0.756
There were no significantdifferences in baseline serum urea, creetinine, urate and lipids between Groups l & II Patients who developed complicationshad sigmficanfiyhigher baseline levels of vWf and fibrin Ddimer, suggesting increased initial endothelial dysfunction and thrombogenesisin these patients, who subsequent"hadadverse outcomes. Endothelial dysfunction end increased thrombogenesis may partly contributeto the vascularcomplicationsof hypertension. Key Words:
End organ damage, myocardial ischemia, population survey
endothelial, dysfunction, thrombogenests,prognosis
joo7
joo8
RELATION BETWEEN CASUAL BLOOD PRESSURE A N D T A R G E T O R G A N D A M A G E IN U N T R E A T E D HYPERTENSIVE COURSE K...T,a k g t g g ~ 3". Okuda, S.Konishi, M. Mukal, K. Matsuzaki, E. Murakami* Hypertension Center, Kinki Central Hospital, 3-1 Kurumazuka, ltami, Hyogo, Japan There is some doubt as to which level of blood pressure begins to damage the target organ in natural course o f essential hypertensive patients. To answer this question, we examined the relation between casual blood pressure and target organ damage in hypertensive patients w h o had never had antihypertensive therapy. We compared the following variables in the cases of 125 hypertensive patients (FIT) who had never had antihypertcnsivc therapy with those in 42 age-matched normotcnsive controls (NT) : electrocardiographic voltage (SVI+RV5), left ventricular wall thickness (LVWT) and LVmass index obtained by the echocardiographic method, ocular fundi finding and serum creatinine (Cr). All hypertensive patients were divided into subgroups according to the level of systolic blood pressure (SBP, each of them having 10 m m H g more than 140 m m H g ) and diastolic blood pressure (DBP, each of them having 5 m m H g more than 90 mmHg). There was a significantly positive correlation between all these variables and BP (SBP and DBP) in FIT. A m o n g the subgroups of HT, SVI+RV5, LVWT, LVmass index, the ocular fundi finding increased significantly in the subgroups at the levels of SBP over 150 m m H g compared with those in NT. The variables in H T were greater than those in N T as D B P had increased (SVI+RV5 ; DBP ~ 90 m m H g , LVmass index and the ocular fundi findings ; DBP ~-- 95 rnmHg, L V W T and Cr ; DBP ~ 105 m m H g ) . These results indicate cardiovascular damage exists in essential hypertensive patients at the levels of casual SBP over 150 m m H g and / or D B P over 95 m m H g in natural course of essential hypertension.
Protective
Key Words: essential hypertension, natural course, target organ damage
Damage
Effect of Benazepril on kidney
in
patients
with essential Hypertension. Tang Shude, Qi Wen Hang, Shanghai Institute of Hypertension, Rui Jin Hospital, Shanghai Second Medical University, 197 Rui Jin Road 2, Shanghai 200025, China. Hypertension is a risky factor for the development of complications such as renal failure. Apart from control of blood pressure, Benazepril, a Long-acting Angiotensin-converting enzyme (ACE) inhibitor has been shown to protect renal function and without affection to blood sugar, serum lipids. 17 cases have been randomly Selected Essential Hypertension (4 Male, 13Female), aged 62.8 4-6.4 years, with mild to moderate essential Hypertension were enrolled into this study, all previors antihypertensive medication was discontined before the start of the study, A baseline siring diastolic blood pressure of /> 95mmHg and ~< 114mmHg and systolic blood pressure of ~< 190mmHg, Blood nitrogen >/ 8mmol/L and blood creatinine />' 120umol/L at the end of plac,cb run-in phase were taken as criteria for study entry. The duration of active treatment with Benazepril was one month. The dose given 10rag to 20rag as a daily dose. After one month active treatment, S B P , D B P , blood Crcatinine , Serum ACE , urinary excretive rates of Immunoglobulin G (lg G) and Micro-Albumin (MAL) decreased obviously (p<0.05-0.01). while urinary excretion rates of Retinol-binding protein are not change (p>0.05). In conclusion, Benazepril a dose daily was sufficient to control blood pressure during the one month treatment period. Benazepril may have a protected effect on kidney in patients with essential Hypertension and improving renal function. Key words: Benazepril essential Hypertension Renal function.
77A
POSTERS:
End Organ
j005
j006
SILENT MYOCARDIAL ISCHEMIA AND THE RELATIONSHIP WITH CARDIOVASCULAR ENDORGAN DAMAGE IN NEWLY FOUND HYPERTENSIVES. W.F. Terpstra I=, J.F. Mayn, A.J. Smit *=, P.A. de Grae~ 2, H.J.G.M. CrijnsL Academic Hospital Groningen ~ and Groningen Hypertension Service =, Groningen, The Netherlands. Hypertension is associated with increased coronary risk. This study was performed to assess the prevalence of asymptomatic ST segment depression and to determine the relationship with cardiovascular end-organ damage in newly found, eldedy hypertensives. From a population survey we included 178 new mild to moderate hypertensives (4x systolic blood pressure _>160 mmHg and/or diastolic blood pressure > 95 mmHg), aged 60 to 75 years with 53% male. Exclusion cdteria were: angina pectoris, severe atherosclerotic disease, diabetes mellitus and ST abnormalities on resting ECG. A 48 hour Holter monitor (3 channel ECG) was performed to detect episodes of ST segment depression, using the 1"1"1 rule of Cohn. Ischemic burden was calculated as number of episodes * total mm* total duration of ST segment depression. Echo left ventricular mass was calculated using the mean of 3 consecutive measurements of septum, posterior wall and end-diastolic diameter and indexed by body surface area (LVMI). Intima-media thickness (IMT) was measured in 10 prespecified segments of carotid and femoral artery. Transient ST segment depression was observed in 21 hypertensive patients, a prevalence of 12 %. In this group, a significant correlation was found between LVMI and ischemic burden (r=0.466:p=0.033). Compared to the group of hypertensives without ST segment depression, LVMI was not significantly different (111 +1-18 vs 104+/-24 g/m =, respectively). However, combined mean far wall IMT was significantly higher in hypertensives demonstrating ST segment depression (0.98+•0.21 vs 0.88+/-0,16 mm; P < 0.05). These data suggest, that vascular endorgan damage is mainly responsible for the development of silent myocardial ischemia in elderly with mild to moderate hypertension. Once myocardial ischemia has developed, an increased demand for oxygen by mass enlargement determines the seventy of myocardial ischemia.
Abnormal Baseline Endothelial Dysfunction end Thrombogenesis are related to Prognosis In Hypertemlon
Key Words:
E Edmu~ds,AD Blann, DG Beevors.GYFILip Hsemostasis Tla'ombo~s end Vascular Biology Unit, University Departmentof Medicine,City Hospital,B i m ~ England Despite high intravascular pressures, the complications of hypertension (heart attacks, sixokes) are p~edoxicully thrombotic rather than haomorrbagic. To inv¢stigatewhether baseline markers of endothelial dysfunction (von Willebrand factor, vWf), baomorheology(haematocrit, fibrinngen,plaranaviscosity),thrombogenesis(fibrin D-dirner),and platelet activation (soluble P-seleetin, sPsel) are related to outcomes, we prospectivelyfollowedup 178 patients (92 males; mean age54.52 sd14.6) with hypertension for a mean of 47.5 months (s.d 10.12). Baseline characteristicsof patients who developed cardiovascularcomplications (angina,myocardialinfarction,ccrebrovascularevents,pcnpheral vascular disease or death) (Group I) (n=24) during follow-up,were compared to thosewho remmned freeof such complications(Group H)
mean(aM.)
Group I SystolicBP nunHg 190.8(24.9) DiastolicBP nunHg 102.9(14.0) Bodymass index keCm2 27.7 (3.7) LV mass index g/m2 177.0(60.1) vWfiU/dl 130.2(31.5) Haeanateerit % 42.5 (4.4) Fibrinogeng/l 3,3 (0.6) ViscositymPa 1.73 (0.11)
Group H 187.4(28.8) 106.0(23.0) 28.5 (47) 154.7(67.2) 111.4(31.2) 42.7 (4.64) 34 ( 1.I ) 1.73 (0.29)
P value 0.57 0.39 0.40 0.17 0.017 0.91 0.61 0.35
250 (175-320) 300 (196-473)
0.018
median (IQR) D-dimerng/ml P-sclectinng/ml
305 (230-500) 260 (165-803)
0.756
There were no significantdifferences in baseline serum urea, creetinine, urate and lipids between Groups l & II Patients who developed complicationshad sigmficanfiyhigher baseline levels of vWf and fibrin Ddimer, suggesting increased initial endothelial dysfunction and thrombogenesisin these patients, who subsequent"hadadverse outcomes. Endothelial dysfunction end increased thrombogenesis may partly contributeto the vascularcomplicationsof hypertension. Key Words:
End organ damage, myocardial ischemia, population survey
endothelial, dysfunction, thrombogenests,prognosis
joo7
joo8
RELATION BETWEEN CASUAL BLOOD PRESSURE A N D T A R G E T O R G A N D A M A G E IN U N T R E A T E D HYPERTENSIVE COURSE K...T,a k g t g g ~ 3". Okuda, S.Konishi, M. Mukal, K. Matsuzaki, E. Murakami* Hypertension Center, Kinki Central Hospital, 3-1 Kurumazuka, ltami, Hyogo, Japan There is some doubt as to which level of blood pressure begins to damage the target organ in natural course o f essential hypertensive patients. To answer this question, we examined the relation between casual blood pressure and target organ damage in hypertensive patients w h o had never had antihypertensive therapy. We compared the following variables in the cases of 125 hypertensive patients (FIT) who had never had antihypertcnsivc therapy with those in 42 age-matched normotcnsive controls (NT) : electrocardiographic voltage (SVI+RV5), left ventricular wall thickness (LVWT) and LVmass index obtained by the echocardiographic method, ocular fundi finding and serum creatinine (Cr). All hypertensive patients were divided into subgroups according to the level of systolic blood pressure (SBP, each of them having 10 m m H g more than 140 m m H g ) and diastolic blood pressure (DBP, each of them having 5 m m H g more than 90 mmHg). There was a significantly positive correlation between all these variables and BP (SBP and DBP) in FIT. A m o n g the subgroups of HT, SVI+RV5, LVWT, LVmass index, the ocular fundi finding increased significantly in the subgroups at the levels of SBP over 150 m m H g compared with those in NT. The variables in H T were greater than those in N T as D B P had increased (SVI+RV5 ; DBP ~ 90 m m H g , LVmass index and the ocular fundi findings ; DBP ~-- 95 rnmHg, L V W T and Cr ; DBP ~ 105 m m H g ) . These results indicate cardiovascular damage exists in essential hypertensive patients at the levels of casual SBP over 150 m m H g and / or D B P over 95 m m H g in natural course of essential hypertension.
Protective
Key Words: essential hypertension, natural course, target organ damage
Damage
Effect of Benazepril on kidney
in
patients
with essential Hypertension. Tang Shude, Qi Wen Hang, Shanghai Institute of Hypertension, Rui Jin Hospital, Shanghai Second Medical University, 197 Rui Jin Road 2, Shanghai 200025, China. Hypertension is a risky factor for the development of complications such as renal failure. Apart from control of blood pressure, Benazepril, a Long-acting Angiotensin-converting enzyme (ACE) inhibitor has been shown to protect renal function and without affection to blood sugar, serum lipids. 17 cases have been randomly Selected Essential Hypertension (4 Male, 13Female), aged 62.8 4-6.4 years, with mild to moderate essential Hypertension were enrolled into this study, all previors antihypertensive medication was discontined before the start of the study, A baseline siring diastolic blood pressure of /> 95mmHg and ~< 114mmHg and systolic blood pressure of ~< 190mmHg, Blood nitrogen >/ 8mmol/L and blood creatinine />' 120umol/L at the end of plac,cb run-in phase were taken as criteria for study entry. The duration of active treatment with Benazepril was one month. The dose given 10rag to 20rag as a daily dose. After one month active treatment, S B P , D B P , blood Crcatinine , Serum ACE , urinary excretive rates of Immunoglobulin G (lg G) and Micro-Albumin (MAL) decreased obviously (p<0.05-0.01). while urinary excretion rates of Retinol-binding protein are not change (p>0.05). In conclusion, Benazepril a dose daily was sufficient to control blood pressure during the one month treatment period. Benazepril may have a protected effect on kidney in patients with essential Hypertension and improving renal function. Key words: Benazepril essential Hypertension Renal function.
77A