青年急性ST段抬高心肌梗死(STEMI)患者危险因素和冠脉造影特点分析

目的 研究青年急性ST段抬高心肌梗死(STEMI)患者的危险因素、临床及冠状动脉病变特点,探讨青年急性心肌梗死的防治.方法 选择经冠脉造影证实的AMI患者190例,根据年龄分组为:年龄≤45岁青年组(A组)60例及年龄≥60岁老年组(B组)130例,比较两组患者的危险因素、临床表现和冠脉造影资料.结果 ①A组患者多有吸烟(80%比30.7%,P＜0.05)及早发冠心病家族史(40%比10.7%,P＜0.05),两组代谢综合征各项指标中仅高密度脂蛋白胆固醇差异有统计学意义(46.6%比38.4%,P＜0.05).基础心功能A组均正常,B组中正常占86.2%,差异具有统计学意义(P＜0.05). A组中AMI后心功能Killip Ⅱ～Ⅳ级占5%,B组为40%(P＜0.05).②A组单支病变发生率高为75%,多侵犯LAD;而B组双支及三支病变发生率高为87%.A组冠脉病变以低中危为主,低危占30%;B组则以中高危为主,高危占18.5%.结论 吸烟、家族遗传因素及低高密度脂蛋白胆固醇是青年STEMI最重要的危险因素.青年急性STEMI冠脉病变以低中危为主,多侵犯左前降支.积极控制上述危险因素,及时经皮冠脉介入再灌注治疗对降低本病发病及改善预后具有非常重要的意义.     

开展经皮冠状动脉成形术前后冠状动脉造影临床应用对比

目的:了解在开展冠状动脉成形水(PTCA)前后冠脉造影在年龄、性别、冠脉病变种类、冠脉粥样硬化情况及其造影适应症等方面的变化.方法:采用回顾性资料分析方法,比较上海中山医院开展PTCA前134例(A组)和开展PTCA后440例(B组)冠脉造影资料上述指标问的差别.结果:(1)60岁以上造影者B组明显高于A组(P<0.05),且B组年龄跨度大于A组.(2)急性心梗冠脉造影者乃明显高于A组(P<0.05),其中B组急诊冠脉造影占18.29%,心梗后早期冠脉造影占28.05%;陈旧性心梗A组明显高于B组(P<0.05).诊断性冠脉造影两组无差别(P>0.05).(3)冠脉病变A组以单支、简单的A型病变为主,B组以多支复杂的B型和C型多见(P<0.05).结论:开展PTCA之后冠脉造影例数显著增加,造影年龄跨度增加12岁,平均年龄上升6.7岁;60岁以上老年人所占比例提高26.05%,冠脉造影适应症较前扩大,但病变阳性率并未下降,冠脉病变趋向多支、复杂的B型和C型.     

青年人急性心肌梗死临床及冠状动脉造影特点分析

目的分析青年人急性心肌梗死(AMI)的临床及冠状动脉(冠脉)造影特点,进一步探讨其可能的发病机制。方法回顾性对照分析51例年龄≤45岁(青年组)及同期205例≥50岁的(非青年组)AMI患者的危险因素及诱因,临床、心电图表现及冠脉造影特点。结果2组患者危险因素存在差异,青年组吸烟明显多于非青年组,心电图ST段抬高性心肌梗死(STEMI)显著高于非青年组,冠脉造影无明显狭窄、A型病变、单支病变者显著高于非青年组。结论青年人AMI常有明显诱因,冠脉造影狭窄程度轻,A型病变及单支病变常见。     

不同年龄急性心肌梗死患者冠脉造影及血管内超声特征研究

目的 观察不同年龄急性心肌梗死(AMI)的冠脉造影和罪犯病变血管内超声(IVUS)特征.方法 入选2003年6月至2006年6月于杭州市第一人民医院行介入治疗的AMI患者236例,其中42例年龄≤50岁分入A组,194例年龄＞50岁分入B组,应用冠脉造影观察冠脉病变特点.冠脉介入治疗前应用IVUS观察14例A组和38例B组AMI患者罪犯病变,测量血管外弹力膜面积,最小管腔面积,斑块面积,狭窄程度,斑块纤维帽厚度,脂核大小,脂核负荷和斑块破裂情况等.结果 吸烟、酗酒和冠心病家族史在A组多见,B组多合并高血压、糖尿病.A组单支血管病变发生率高,而B组多支血管病变发生率高且侧支循环形成多;IVUS发现2组罪犯病变均主要表现为斑块不稳定和破裂,部分A组患者冠脉血管无严重病变,A组血管病变脂核大,纤维帽薄,B组罪犯病变狭窄程度重,斑块面积大,纤维帽厚度较厚,脂核较小.结论 AMI主要由于斑块不稳定和破裂所致,不同年龄AMI冠脉病变特征和危险因素不同,提示不同年龄患者预防AMI各有侧重.     

血清ox-LDL、ApoB及ApoB/A1与早发冠脉三支病变发生的关系

目的 探讨早发冠脉三支病变患者血清氧化低密度脂蛋白(ox-LDL)、载脂蛋白B(ApoB)、载脂蛋白A1( ApoA1)及ApoB/A1的特点.方法 共选取冠心病(CHD)患者164例,根据冠脉造影结果分为早发冠脉三支病变组96例(观察组),冠脉正常组(对照组)68例,比较两组患者血脂水平、ox-LDL、及ApoA1、ApoB的水平,分析其与早发冠脉三支病变的关系.结果 观察组血清ox-LDL、ApoB、ApoB/A1水平高于对照组(P＜0.01);而观察组与对照组血清ApoA1水平比较无统计学差异.Logistic回归分析显示,ox-LDL在两组患者中存在统计学差异(P＜0.05).结论 血清ox-LDL、ApoB、ApoB/A1水平是早发冠脉三支病变发生的预测因素,其中ox-LDL是预测早发严重冠脉三支病变发生的独立危险因素.     

不同性别冠心病患者冠脉病变特点及发病危险因素分析

目的观察不同性别冠心病(CHD)患者冠脉病变特点及心血管传统、非传统危险因素的差别。方法收集住院的CHD患者451例,比较男、女性CHD患者传统及非传统危险因素、冠状动脉病变支数、CHD类型、相关生化指标的差异。结果①在CHD传统危险因素中,男性患者吸烟所占比率显著高于女性(P<0.05),女性患者年龄在60岁及以上的显著多于男性;②在CHD非传统危险因素中,男性患者的超敏C反应蛋白水平明显增高,女性患者的高密度脂蛋白胆固醇、载脂蛋白A1、载脂蛋白B/载脂蛋白A1水平和腹型肥胖与男性比较有显著差异(P<0.05)。③男性患者冠脉病变以多支为主,病变类型以急性心肌梗死为主,与女性患者差异有统计学意义(P<0.05)。结论不同性别CHD患者发病的传统危险因素、非传统危险因素、冠脉病变支数、病变类型都有差别,应重视非传统危险因素的价值。     

12294例不同年龄患者冠状动脉造影的特征及危险因素研究

目的观察不同年龄患者冠状动脉造影特征,分析其危险因素及病变特点。方法选择拟诊冠心病行冠状动脉造影的患者12294例,根据年龄将<60岁患者作为A组(6520例),≥60岁患者作为B组(5774例)。应用冠状动脉造影观察冠状动脉病变特点。结果A组男性多见,多具有吸烟习惯和冠心痛家族史,B组多合并高血压、糖尿病和高脂血症。A组单支病变发生率高,而B组多支病变发生率高。结论不同年龄的患者冠状动脉病变特征和危险因素不同,提示不同年龄患者预防冠心病各有侧重。     

冠状动脉造影正常的急性心肌梗死患者临床预后的研究

目的　通过对冠状动脉 (冠脉 )造影正常的急性心肌梗死 (MINC)患者的随访 ,探讨其临床预后 ,并分析发病危险因素。方法　 1987至 2 0 0 1年北京大学第一医院 4 0例 (A组 )首次急性心肌梗死后冠脉造影正常 (冠脉造影狭窄程度小于 2 0 % )患者。同时随访了 12 9例 (B组 )年龄、性别、梗死部位与A组相匹配的冠脉造影严重狭窄 (梗死相关血管狭窄程度 >5 0 % )的急性心肌梗死患者 ,比较分析两组患者急性期、远期预后及发病危险因素。结果　高血压史、危险因素个数、梗死后心绞痛发生率A组明显低于B组。住院期间LVEFA组明显高于B组。两组患者平均随访时间相似 (6 7± 4 0比 6 8± 34月 )。复合心血管事件发生率A组明显少于B组。结论　MINC患者急性期、远期预后明显好于MICS患者 ,冠心病危险因素明显少于后者     

冠状动脉造影确诊的中、老年冠心病患者的危险因素比较

目的 比较中、老年冠心病病人危险因素情况。方法选冠状动脉造影确诊的冠心病病人105例,其中≥40岁而<60岁的中年组(A组)65例,≥60岁的老年组(B组)40例,就以下6个危险因素:高血压、糖尿病、高纤维蛋白原、吸烟史、阳性家族史及高脂血症进行比较。结果高血压、糖尿病和高纤维蛋白原(Fig),A组少于B组;吸烟史及阳性家族史A组明显多于B组;高脂血症两组问无显著差异。有3个以上危险因素者共63例,A组41例,占该组63.08％,B组22例,占该组55.00％,两组间差异无显著性。结论 中年组冠心病病人吸烟史、阳性家族史、高脂血症为主要危险因素。老年组病人应控制血糖、血脂、降压、降纤维蛋白原,对冠心病危险因素应综合治疗,预防为主。     

多支慢性冠状动脉闭塞病变侧支循环形成的影响因素分析

目的探讨影响慢性冠状动脉闭塞病变(CTO)多支病变侧支循环形成的因素。方法选择2003—2008年沈阳市第四人民医院心血管内科40例既往无心肌梗死的CTO患者,分为侧支良好组(A组)和侧支不良组(B组)。对两组患者的冠脉造影特点、临床特征进行对比分析。结果 A组中左优势冠脉即回旋支粗大占67.8%,B组中左优势冠脉仅占25.0%(P0.05),A组近端病变患者明显多于B组(P0.01),心绞痛病程(3个月)在A组中占96.4%,在B组中占66.6%(P0.05)。多因素logistic回归分揭示冠脉近端病变和糖尿病是良好侧支循环形成与否的独立影响因素。结论冠脉近端部位闭塞及左优势冠脉类型易于在CTO多支病变中建立侧支循环,心绞痛病程(3个月)时侧支循环明显增多,冠脉近端病变和糖尿病是侧支循环形成的独立影响因素。     

Angiographic correlates of anterior ST segment depression in acute inferior wall myocardial infarction.

This study was conducted prospectively to assess the correlation between the pattern of anterior ST segment depression on the admission electrocardiogram and the in-hospital morbidity and mortality in patients with acute inferior wall myocardial infarction. Coronary angiography was also done to assess its correlation, if any, with pattern of anterior ST segment depression. Our study cohort comprised of 165 consecutive patients with acute inferior wall myocardial infarction divided into four groups based on admission electrocardiogram. Group I (n = 33): patients with no anterior ST segment depression; group II (n = 16): patients with ST segment depression in leads V1-V3; group III (n = 71): patients with ST segment depression in leads V4-V6, I and aVF, and; group IV (n = 45): patients with ST segment depression in all anterior leads (V1-V6, I, aVL). The outcomes were analysed in terms of high grade atrioventricular block, Killip class II or higher failure, and in-hospital mortality. Coronary angiography was performed to analyse coronary anatomy. Group IV patients had increased incidence of complete heart block (37.8% vs 15.2% in the total group) (p < 0.001) and increased mortality (11.1% vs 4.2% in the total group) (p < 0.05). This group also had greater incidence of triple vessel disease (76.7%) (p < 0.001). Group II patients had greater incidence of double vessel disease (88.9%) (p < 0.05) and had no triple vessel disease. Group III patients had double vessel disease (76.5%) (p < 0.05) or triple vessel disease (23.5%) (p = NS) and no single vessel disease. Coronary angiography in group II showed greater incidence of involvement of left circumflex artery and right coronary artery while in group III there was left anterior descending artery and right coronary artery disease. We conclude that patients with anterior ST segment depression in group III and group IV categories are in high risk subset with acute inferior wall myocardial infarction.     

Significance of precordial ST-segment depression in acute transmural inferior infarction: Coronary angiographic findings

Coronary arteriographic findings in patients with acute transmural inferior infarction were studied from 57 patients (51 men and 6 women). Their ages ranged from 28 to 72 years with a mean of 50 years. Twenty-six patients (Group A) had minimal (less than 0.1 mV) or no precordial ST-segment depression. Thirty-one patients (Group B) had precordial ST-segment depression of 0.1 mV or more. The two groups showed consistent differences in frequency of the left anterior descending artery (LAD) stenosis, multivessel disease, mean peak plasma creatinine phosphokinase (CPK, IU/L), and mean ejection fraction. For Group A vs B, these differences were: LAD stenosis, 31% vs 68%, multivessel disease, 35% vs 81%, mean peak plasma CPK, 1283 versus 1904, and mean ejection fraction, 60.5% vs 45.3%. The incidence of abnormal anterolateral and posterobasal wall motion in Group B was more (p < 0.01 and p < 0.05 respectively) than in Group A. All patients in Group B who had precordial ST-segment depression of 0.3 mV or greater, had LAD stenosis. There was no relation between the duration of ST-segment depression and the presence of LAD stenosis. Also, there was no correlation between the presence of collateral circulation and the development of ST-segment depression. The Group B patients tended to have more complications in the acute phase and in the follow up period (p < 0.05) than did those in Group A. It is concluded that precordial ST-segment depression in acute inferior wall infarction is probably related to anterior injury due to LAD stenosis and these patients were shown to have more severe coronary artery disease, more depression of their ejection fractions, and more myocardial damage than patients without this finding. The earliest recorded ECG is most valuable in identifying the high risk patients. The presence of LAD stenosis in patients with inferior wall infarction who have precordial ST-segment depression of 0.3 mV or more are likely.     

Left anterior descending coronary artery obstruction. Clinical, electrocardiographic, and angiographic correlates.

Seventy-six patients with severe (greater than 80%) occlusive left anterior descending coronary artery disease by coronary angiography were examined for the electrocardiographic characteristics of this disease in the presence (group A 59 patients) or the absence (group B 17 patients) of anterior wall asynergy (akinesis or dyskinesis). The incidence of clinically documented anterior myocardial infarction in these two groups of patients was examined. The collateral circulation to the left anterior descending coronary artery was also examined in the groups of patients with and without anterior wall asynergy. Thirty-eight of 59 (64%) patients with anterior wall asynergy (group A) showed electrocardiographic signs of anterior myocardial infarction, 17 per cent showed probable electrocardiographic signs of anterior myocardial infarction and 19 per cent showed no electrocardiographic signs. None of the 17 patients without anterior wall asynergy (group B) showed electrocardiographic signs of anterior myocardial infarction. In group A 74.6 per cent had documented clinical evidence of previous anterior myocardial infarction. Collateral filling of the distal left anterior descending coronary artery was seen in 71 per cent of group A and 100 per cent of group B patients. There was a significantly higher incidence (P = 0.02) of collateral filling in the patients without electrocardiographic evidence of definite anterior myocardial infarction (93% of 28 patients), than in those who showed definite electrocardiographic evidence of anterior myocardial infarction (66% of 38 patients).it is concluded that severe occlusive left anterior descending coronary artery disease with anterior wall myocardial asynergy is usually associated with electrocardiographic signs of anterior myocardial infarction, whereas equally severe left anterior descending coronary artery disease without anterior wall asynergy is rarely associated with electrocardiographic abnormalities of anterior myocardial infarction. Severe left anterior descending coronary artery obstruction without electrocardiographic and angiographic evidence of anterior myocardial infarction is usually associated with collateral circulation to the left anterior descending coronary artery and collateral circulation to the left anterior descending coronary artery is present less frequently when obstruction is associated with anterior myocardial infarction.     

Left anterior descending coronary artery obstruction. Clinical, electrocardiographic, and angiographic correlates.

Seventy-six patients with severe (greater than 80%) occlusive left anterior descending coronary artery disease by coronary angiography were examined for the electrocardiographic characteristics of this disease in the presence (group A 59 patients) or the absence (group B 17 patients) of anterior wall asynergy (akinesis or dyskinesis). The incidence of clinically documented anterior myocardial infarction in these two groups of patients was examined. The collateral circulation to the left anterior descending coronary artery was also examined in the groups of patients with and without anterior wall asynergy. Thirty-eight of 59 (64%) patients with anterior wall asynergy (group A) showed electrocardiographic signs of anterior myocardial infarction, 17 per cent showed probable electrocardiographic signs of anterior myocardial infarction and 19 per cent showed no electrocardiographic signs. None of the 17 patients without anterior wall asynergy (group B) showed electrocardiographic signs of anterior myocardial infarction. In group A 74.6 per cent had documented clinical evidence of previous anterior myocardial infarction. Collateral filling of the distal left anterior descending coronary artery was seen in 71 per cent of group A and 100 per cent of group B patients. There was a significantly higher incidence (P = 0.02) of collateral filling in the patients without electrocardiographic evidence of definite anterior myocardial infarction (93% of 28 patients), than in those who showed definite electrocardiographic evidence of anterior myocardial infarction (66% of 38 patients).it is concluded that severe occlusive left anterior descending coronary artery disease with anterior wall myocardial asynergy is usually associated with electrocardiographic signs of anterior myocardial infarction, whereas equally severe left anterior descending coronary artery disease without anterior wall asynergy is rarely associated with electrocardiographic abnormalities of anterior myocardial infarction. Severe left anterior descending coronary artery obstruction without electrocardiographic and angiographic evidence of anterior myocardial infarction is usually associated with collateral circulation to the left anterior descending coronary artery and collateral circulation to the left anterior descending coronary artery is present less frequently when obstruction is associated with anterior myocardial infarction.     

Implications of acute left ventricular remodeling during squatting stress echocardiography

Background: We previously demonstrated that squatting induces left ventricular (LV) wall motion abnormalities (WMA) in areas subtended by stenotic coronary arteries. In addition, it was observed that some subjects developed acute changes in LV shape (acute left ventricular remodeling [ALVRM]) during squatting. Objective: This study tested the hypothesis that patients with ALVRM during squatting echocardiography have higher incidences of severe coronary artery disease (CAD). Methods: Echocardiography was performed in all standard views during standing and squatting. End‐systolic frames in the apical four‐chamber view were analyzed. Results: The subjects were divided into three groups. Group 1 consisted of 12 subjects who developed squatting‐induced ALVRM with apical and distal posterior septal akinesis, dilation of the apex and marked LV shape change at end‐systole. Group 2 consisted of 20 subjects with distal posterior septal and apical akinesis without ALVRM, during squatting. Group 3 consisted of 64 subjects who developed WMA in areas other than the apex (n = 49), or normal wall motion (n = 15) during squatting. Coronary angiography in group 1 revealed that 6 subjects had left main coronary artery stenosis (LMCAS ≥ 50%), two had severe three vessel disease (≥90% stenosis), and one had 100% left anterior descending coronary artery occlusion. Severe CAD was defined for purpose of this study as the presence of LMCAS, or severe three vessel disease (≥90% stenosis). Six subjects in group 2 had LMCAS and none had severe three vessel disease (P < 0.05 vs. group 1 for LMCAS and/or three vessel disease). In group 3, eight had LMCAS and none had severe three vessel disease (P < 0.0001 vs. group 1). Conclusion: Patients with ALVRM have severe CAD. Therefore, patients who develop ALVRM during squatting require urgent evaluation for revascularization therapy. (Echocardiography 2012;29:700‐705)     

Coronary artery ectasia: angiographic, clinical profile and follow-up

Out of 3200 coronary angiograms we reviewed, there were 144 cases of coronary ectasia--an incidence of 4.5 percent. Among these, 122 were associated with atherosclerotic coronary artery disease, i.e. coronary stenosis more than 50 percent (group A) and 22 not associated with coronary artery disease (group B). The patients in groups A and B were compared with age- and sex-matched patients (group C) (n=100) who had coronary artery disease alone without ectasia. The incidence of ectasia was not increased in patients with thoracoabdominal aortic aneurysm i.e. 2/154 (1.8%) or in patients with peripheral occlusive vascular disease i.e. 5/161 (3.1%). Ectasia was typed according to a modified version of the criteria proposed by Markis et al. Type II was the commonest, followed by type I, III and IV. Right coronary artery was the most commonly involved vessel by ectasia followed by left circumflex, left anterior descending artery and left main coronary artery. Diffuse ectasia was seen more frequently in right coronary artery and localised ectasia in left anterior descending artery. Patients in groups A and B had similar epidemiological characteristics, though more patients with ectasia alone (group B) had better left ventricular function and negative stress tests. The patients in group A had a similar incidence of previous myocardial infarction, coronary risk factor profile, treadmill exercise test status and severity of coronary artery disease when compared to group C. On a mean follow-up of 3+/-1.2 years, all the three groups had similar event rates.     

Left ventricular function after myocardial infarction: clinical and angiographic correlations

There is a paucity of information correlating the angiographic findings immediately after myocardial infarction with the clinical status before infarction. Therefore, the coronary anatomy, collateral circulation and quantitative left ventricular function were studied in 39 patients who underwent angiography within 3 weeks of a first transmural myocardial infarction. In all patients, the vessel supplying the infarct was totally occluded at the time of angiography. Patients without angina before infarction (Group I) had fewer coronary obstructions than did patients with a long history of angina before infarction (Group II) (1.5 +/- 0.5 versus 2.5 +/- 0.5, respectively, p less than 0.001) but worse overall and regional left ventricular function. These paradoxical differences between Groups I and II were evident in patients with anterior as well as inferior infarction. Patients in Group I had significantly lower collateral scores than did patients in Group II (0.6 +/- 0.8 versus 1.9 +/- 0.9, respectively, p less than 0.0001) and 13 of 22 patients in Group I had no collateral vessels compared with only 1 of 17 in Group II (p less than 0.001). Partial preservation of anterior wall function in Group II patients with anterior infarction was related both to the presence of collateral vessels and to the more distal obstruction of the left anterior descending coronary artery in these patients as compared with patients with anterior infarction in Group I. In contrast, in patients with inferior wall infarction, no relation could be found between the presence of collateral vessels and regional left ventricular function, although only two patients in this series with inferior infarction did not have collateral vessels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Detection of disease of the anterior interventricular artery by 2-dimensional echocardiography in acute inferior infarction. Comparison with the electrocardiographic data

The authors report their experience of 2D echocardiography in the acute stage of myocardial infarction. One hundred patients, 60 men and 40 women, aged 60 +/- 4.5 years (range 32 to 69 years) were admitted to hospital with an uncomplicated inferior myocardial infarction and underwent 2D echocardiography on admission and coronary angiography 15 days later. Ten patients were excluded because unsatisfactory quality of the echocardiographic images. Forty-seven patients had initial ST depression of at least 1 mm in leads V1 to V4 (Group I) and 43 patients did not show these electrical changes (Group II). There were no significant differences in the clinical findings or in the cardiovascular risk factors between the 2 groups. On the other hand, inaugural necrosis was commoner in Group II (p less than 0.03) and cardiomegaly and CPK elevation greater in Group I (p less than 0.02). 2D echocardiography demonstrated the same degree of posterior wall hypokinesia or akinesia in the 2 groups. Septal hypokinesia was observed twice as commonly in Group I (p less than 0.03) both at echocardiography and ventriculography. Haemodynamic and angiographic data showed that double and triple vessel disease was commoner (p less than 0.05), that left anterior descending disease was more severe (p less than 0.03), left ventricular end diastolic pressure was higher (p less than 0.02) and the ejection fraction lower (p less than 0.02) in Group I, compared with Group II.(ABSTRACT TRUNCATED AT 250 WORDS)