中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2013年
9期
761-765
,共5页
达娃次仁%格桑罗布%卓玛次仁%李奎%古桑拉姆%张令军%次旦罗布%格桑嘎瓦%达瓦
達娃次仁%格桑囉佈%卓瑪次仁%李奎%古桑拉姆%張令軍%次旦囉佈%格桑嘎瓦%達瓦
체왜차인%격상라포%탁마차인%리규%고상랍모%장령군%차단라포%격상알와%체와
心脏病%高血压,肺性%心脏损伤
心髒病%高血壓,肺性%心髒損傷
심장병%고혈압,폐성%심장손상
Heart disease%Hypertention,pulmonary%Hear injuries
目的 了解慢性高原心脏病(HAHD)不同程度肺动脉高压(PAH)患者心脏结构及功能的变化.方法 对2010年1月至2011年1月我院收治的99例HAHD患者根据超声心动图估测肺动脉收缩压(PASP)水平,将PAH分为轻度:30～49 mm Hg(1 mm Hg=0.133 kPa);中度:50 ～ 69mm Hg；重度:70 mm Hg以上三组,对各组患者心脏结构、心功能、心律失常情况及全血N末端B型利钠肽原(NT-proBNP)水平等进行比较.另选同期入院无明确器质性疾病者50例作对照组.结果 右心室前壁厚度在中、重度PAH组较对照组显著增加[(5.10±2.23)、(7.00±2.29)mm比(3.70±0.92) mm,P＜0.05],重度PAH组较轻、中度PAH组也显著增加[(7.00±2.29) mm比(4.58±1.80)、(5.10 ±2.23)mm,P＜0.05],但轻度PAH组与对照组之间差异无统计学意义；HAHD右心室内径在轻、中、重度PAH组较对照组显著增加[(24.36±4.99)、(27.68 ±5.45)、(29.72 ±5.18)mm比(17.64 ±2.88) mm,P＜0.01],右心室流出道内径在轻、中、重度PAH组较对照组显著增加[(27.62±5.40)、(30.95 ±6.18)、(29.91±5.38)mm比(24.67±3.98) mm,P＜0.01].中、重度PAH组较轻度PAH组也有显著增加(P＜0.01).心室间隔厚度在轻、中、重度PAH组较对照组显著增加[(8.78±1.45)、(9.77±1.38)、(9.82±1.5 3)mm比(7.98±1.47)mm,P＜0.05].左心房前后径轻、中、重度PAH组较对照组显著增加(P＜0.05),但在各PAH组之间差异无统计学意义.左心室射血分数在HAAD轻、中、重度PAH组较对照组显著下降[(67.26±8.76)、(60.24±13.78)、(63.95±11.50) mm比(71.40 ±7.41)mm,P＜0.05],中度PAH组较轻度PAH组进一步下降(P＜0.05),但在重度PAH组较中度PAH组反而有所升高[(63.95±11.50) mm比(60.24±13.78) mm,P ＞0.05].单因素相关分析显示,lgPASP与左心室射血分数(R=-0.103,P=0.298)无显著相关性.HAHD与对照组比较临床心功能失代偿及心律失常的出现率显著升高(P＜0.05)；全血NT-proBNP水平随着PASP的升高而进行性增加,且各组之间差异均有统计学意义(P＜0.05).结论 HAHD者随着PASP的升高右心结构与功能发生显著改变,同时左心结构及功能也出现轻度异常.
目的 瞭解慢性高原心髒病(HAHD)不同程度肺動脈高壓(PAH)患者心髒結構及功能的變化.方法 對2010年1月至2011年1月我院收治的99例HAHD患者根據超聲心動圖估測肺動脈收縮壓(PASP)水平,將PAH分為輕度:30～49 mm Hg(1 mm Hg=0.133 kPa);中度:50 ～ 69mm Hg；重度:70 mm Hg以上三組,對各組患者心髒結構、心功能、心律失常情況及全血N末耑B型利鈉肽原(NT-proBNP)水平等進行比較.另選同期入院無明確器質性疾病者50例作對照組.結果 右心室前壁厚度在中、重度PAH組較對照組顯著增加[(5.10±2.23)、(7.00±2.29)mm比(3.70±0.92) mm,P＜0.05],重度PAH組較輕、中度PAH組也顯著增加[(7.00±2.29) mm比(4.58±1.80)、(5.10 ±2.23)mm,P＜0.05],但輕度PAH組與對照組之間差異無統計學意義；HAHD右心室內徑在輕、中、重度PAH組較對照組顯著增加[(24.36±4.99)、(27.68 ±5.45)、(29.72 ±5.18)mm比(17.64 ±2.88) mm,P＜0.01],右心室流齣道內徑在輕、中、重度PAH組較對照組顯著增加[(27.62±5.40)、(30.95 ±6.18)、(29.91±5.38)mm比(24.67±3.98) mm,P＜0.01].中、重度PAH組較輕度PAH組也有顯著增加(P＜0.01).心室間隔厚度在輕、中、重度PAH組較對照組顯著增加[(8.78±1.45)、(9.77±1.38)、(9.82±1.5 3)mm比(7.98±1.47)mm,P＜0.05].左心房前後徑輕、中、重度PAH組較對照組顯著增加(P＜0.05),但在各PAH組之間差異無統計學意義.左心室射血分數在HAAD輕、中、重度PAH組較對照組顯著下降[(67.26±8.76)、(60.24±13.78)、(63.95±11.50) mm比(71.40 ±7.41)mm,P＜0.05],中度PAH組較輕度PAH組進一步下降(P＜0.05),但在重度PAH組較中度PAH組反而有所升高[(63.95±11.50) mm比(60.24±13.78) mm,P ＞0.05].單因素相關分析顯示,lgPASP與左心室射血分數(R=-0.103,P=0.298)無顯著相關性.HAHD與對照組比較臨床心功能失代償及心律失常的齣現率顯著升高(P＜0.05)；全血NT-proBNP水平隨著PASP的升高而進行性增加,且各組之間差異均有統計學意義(P＜0.05).結論 HAHD者隨著PASP的升高右心結構與功能髮生顯著改變,同時左心結構及功能也齣現輕度異常.
목적 료해만성고원심장병(HAHD)불동정도폐동맥고압(PAH)환자심장결구급공능적변화.방법 대2010년1월지2011년1월아원수치적99례HAHD환자근거초성심동도고측폐동맥수축압(PASP)수평,장PAH분위경도:30～49 mm Hg(1 mm Hg=0.133 kPa);중도:50 ～ 69mm Hg；중도:70 mm Hg이상삼조,대각조환자심장결구、심공능、심률실상정황급전혈N말단B형리납태원(NT-proBNP)수평등진행비교.령선동기입원무명학기질성질병자50례작대조조.결과 우심실전벽후도재중、중도PAH조교대조조현저증가[(5.10±2.23)、(7.00±2.29)mm비(3.70±0.92) mm,P＜0.05],중도PAH조교경、중도PAH조야현저증가[(7.00±2.29) mm비(4.58±1.80)、(5.10 ±2.23)mm,P＜0.05],단경도PAH조여대조조지간차이무통계학의의；HAHD우심실내경재경、중、중도PAH조교대조조현저증가[(24.36±4.99)、(27.68 ±5.45)、(29.72 ±5.18)mm비(17.64 ±2.88) mm,P＜0.01],우심실류출도내경재경、중、중도PAH조교대조조현저증가[(27.62±5.40)、(30.95 ±6.18)、(29.91±5.38)mm비(24.67±3.98) mm,P＜0.01].중、중도PAH조교경도PAH조야유현저증가(P＜0.01).심실간격후도재경、중、중도PAH조교대조조현저증가[(8.78±1.45)、(9.77±1.38)、(9.82±1.5 3)mm비(7.98±1.47)mm,P＜0.05].좌심방전후경경、중、중도PAH조교대조조현저증가(P＜0.05),단재각PAH조지간차이무통계학의의.좌심실사혈분수재HAAD경、중、중도PAH조교대조조현저하강[(67.26±8.76)、(60.24±13.78)、(63.95±11.50) mm비(71.40 ±7.41)mm,P＜0.05],중도PAH조교경도PAH조진일보하강(P＜0.05),단재중도PAH조교중도PAH조반이유소승고[(63.95±11.50) mm비(60.24±13.78) mm,P ＞0.05].단인소상관분석현시,lgPASP여좌심실사혈분수(R=-0.103,P=0.298)무현저상관성.HAHD여대조조비교림상심공능실대상급심률실상적출현솔현저승고(P＜0.05)；전혈NT-proBNP수평수착PASP적승고이진행성증가,차각조지간차이균유통계학의의(P＜0.05).결론 HAHD자수착PASP적승고우심결구여공능발생현저개변,동시좌심결구급공능야출현경도이상.
Objective To compare the cardiac structural and functional changes in high altitude heart disease (HAHD) patients with various grade of pulmonary artery hypertension (PAH).Methods Pulmonary artery systolic pressure (PASP) was evaluated by Doppler echocardiography in 100 patients with HAHD and patients were divided into 3 groups:mild (PASP:30-49 mm Hg),moderate (PASP:50-69mm Hg) and severe (PASP ≥70 mm Hg) PAH and 50 patients without organic heart disease served as control group.Data on heart structure and function,heart rhythm and whole blood NT-proBNP were compared among groups.Results Right ventricular free wall was significantly thicker in moderate and severe PAH groups than in the control group [(5.10 ± 2.23) mm,(7.00 ± 2.29) mm vs.(3.70 ± 0.92) mm,P ＜0.05],and in the severe PAH group than in mild and moderate PAH groups [(7.00 ± 2.29)mm vs.(4.58 ± 1.80) mm,(5.10 ±2.23) mm,all P ＜0.05] and which was similar between the mild PAH group and the control group.Right ventricular inter diameter and right ventricular outflow tract inter diameter were significantly increased in all HAHD groups compared to the control group (all P ＜ 0.01),and were also significantly increased in moderate and severe PAH groups than in the mild PAH group (P ＜ 0.01).Thickness of interventricular septum was also significantly increased in HAHD patients than control group and in moderate and severe PAH groups than in moderate PAH group.Left atrium anterior-posterior diameter was significantly increased in HAHD patients than in control group and was similar among HAHD patients with various degree of PAH.Left ventricular ejection fraction (LVEF) was remarkably decreased in all HAHD groups than in the control group (P ＜ 0.05),moreover,LVEF was remarkably decreased in the moderate PAH group than in the mild PAH group (P ＜ 0.05).EF was similar between severe PAH group and moderate PAH group (P ＞ 0.05).There was no significant correlation between lgPASP and EF (R =-0.103,P =0.298).Compared with the control group,the incidences of decompensated heart failure and arrhythmia were remarkably increased in HAHD patients (P ＜ 0.05).The level of whole blood NT-proBNP increased in proportion to increasing PASP in HAHD patients (P ＜ 0.05).Conclusion Increased PASP correlates with whole blood NT-proBNP and is an important determinant affecting the fight ventricular structure and left and right ventricular function in HAHD patients.
