Quantification of carotid atheroma, by vascular ultrasonics and spectral analysis, after myocardial infarction. Apropos of 80 cases

A prospective study of carotid artery atheroma by vascular echotomography and spectral analysis was performed in 40 patients with myocardial infarction and 40 control subjects. Carotid artery atheroma was commoner in the group of patients with myocardial infarction (72.5% +/- 6.8%), earlier (9 years), more commonly bilateral (37.5% +/- 7.6%) and more stenotic (32.5% +/- 7.4%) than in the control group (p less than 0.000a, p less than 0.0001 and p less than 0.002, respectively). The severity of carotid artery atheroma correlated with the site of coronary artery disease; the following significant relationships were found: stenosing 40% and/or bilateral carotid atherosclerosis and left anterior descending disease (p less than 0.02); carotid atherosclerosis and double or triple vessel disease (p less than 0.05). The authors conclude that detection of carotid artery atheroma after myocardial infarction is valuable for two reasons: it gives an indication as to the severity of the coronary disease; carotid endarterectomy may be considered at the same time as coronary artery bypass surgery.     

Myocardial infarction in the young subject: a medium-term clinical and coronary angiographic study in 40 patients under 36 years of age. Comparison with coronary angiographic data of myocardial infarction in patients after 50 years of age

A series of 40 myocardial infarctions, occurring in patients under 36 years of age was studied retrospectively (Group I: mean age 31.3 years). The medium term results of coronary angiography in this group were compared with those of 60 myocardial infarctions after 50 years of age (Group II: mean age 56.6 years). Group I had a clear male predominance (92.5%), a high incidence of smoking (69%), hypercholesterolaemia (69%); myocardial infarction was the first manifestation of their disease in 54% and it was often extensive (42%). A comparative angiographic study between the two groups showed: 1) Less widespread lesions in Group I, as assessed by the number of main arteries stenosed (p less than 0.001), the coronary index (p less than 0.01) and the mean coronary score using Friesinger's method (p less than 0.01). 2) A higher incidence of subnormal coronary angiogrammes in Group I (absence of 50% stenosis) (15%) and of single vessel disease (40%): compared with Group II in which multivessel disease was observed in 86.5% of cases. 3) Collateral circulation was less common in Group I (p less than 0.01). On the other hand, a comparative study of regional and global left ventricular function showed no difference between the two groups. Two subgroups were distinguished in Group I: in one subgroup, multiple lesions similar to those found in Group II, suggestive of premature coronary atherosclerosis (52.5%); the other group (47.5%) presented unilocular lesions i.e. focal mono-arterial lesions compatible with other causes of infarction (thrombosis and/or spasm). These patients were younger (p less than 0.05) and had significantly fewer cardiovascular risk factors (p less than 0.01). Despite the fact that the coronary lesions were limited, the myocardial damage was comparable with the other groups as the collateral circulation was much less developed (p less than 0.02). These appearances were only observed in 3.5% of patients in Group II. The study of the angiographic outcomes of these two types of lesions should show a difference and could contribute to the understanding of their mechanisms.     

Higher Gensini score of coronary arteries in acute inferior myocardial infarction with precordial ST-segment depression.

To investigate the significance of precordial ST-segment depression in acute inferior myocardial infarction, we compared the Gensini score of coronary artery stenosis between 2 groups of patients with and without precordial ST-segment depression. Group I consisted of 28 patients who showed ST-segment depression on admission (greater than or equal to 1 mm in V2-V6) and Group II (n = 16) those without ST-segment depression (less than 1 mm). The Gensini score of the coronary arteries (56 +/- 29 vs. 28 +/- 18; p less than 0.001), the partial score of the infarction-related artery (29 +/- 16 vs. 17 +/- 11; p less than 0.01) and of the infarction-nonrelated artery (27 +/- 24 vs. 11 +/- 12; p less than 0.02) were significantly higher in Group I than in Group II. The Killip score (greater than or equal to II) (34% vs. 6%; p less than 0.05), frequency of arrhythmias (75% vs. 38%; p less than 0.02) and peak CK value (3,676 +/- 2,290 vs. 1,818 +/- 1,153 IU/L; p less than 0.005) were higher in Group I than in Group II. Four patients in Group I died following admission, while no patient died in Group II (N.S.). Autopsy findings from the 4 Group I patients revealed fresh extensive inferior infarction and healed diffuse subendocardial infarction which could not be predicted from electrocardiograms. All patients who survived the acute stage performed treadmill exercise testing and 22 patients underwent exercise thallium-201 single photon emission computer tomography (SPECT). On treadmill exercise test, there was no significant difference between the 2 groups in the frequency of angina pectoris and ST-segment depression. On SPECT, the perfusion defect area under 55% of maximum uptake at the redistribution phase was 45.8 +/- 19.6 cm2 in Group I (n = 14) and 34.7 +/- 21.3 cm2 in Group II (n = 8; N.S.). In conclusion, precordial ST-segment depression in acute inferior myocardial infarction suggested advanced atherosclerosis in both the infarction-related and nonrelated coronary arteries, indicating a larger infarct size.     

Clinical correlates of coronary cineangiography in young males with myocardial infarction.

Thirty-eight men who suffered acute transmural myocardial infarction before age 40, and after recovery were New York Heart Association functional Class I or II, were studied by noninvasive means and by coronary angiography in order to determine whether these nonivasive studies could predict the presence of significant coronary artery disease remote from that felt to be responsible for the previous myocardial infarction. Patients were divided into two groups on the basis of the absence (Group I) or presence (Group II) of obstructive disease in a major coronary artery supplying myocardium remote from the prior myocardial infarction. There were 21 patients in Group I and 17 patients in Group II. They did not differ with respect to age, abnormalities of lipid or glucose metabolism, family history, history of hypertension or cigarette use, presence of obesity, or infarct localization. Ten of 17 patients in Group II had angina pectoris; only 3/21 patients in Group I had angina pectoris (p less than 0.01). All 12 patients tested in Group II had a positive maximal exercise tolerance test; only 1/17 patients tested in Group I was similarly positive (p less than 0.001). The absence of angina pectoris and the presence of a negative maximal exercise tolerance test is strong evidence against the pressure of significant CAD remote from that responsible for the prior myocardial infarction.     

颈动脉粥样硬化斑块稳定性与脑梗死的相关研究

目的探讨颈动脉粥样硬化斑块的稳定性与脑梗死关系。方法对120例脑梗死病人及100例对照组病人行颈动脉超声检查。结果脑梗死组斑块发生率（72．8％）明显高于对照组（56．0％），梗死组不稳定斑块（软斑及溃疡斑）的发生率明显高于对照组（分别为41．1％与18．3％）；梗死侧组软斑及溃疡斑的发生率亦明显高于非梗死侧组，分别为63个（52.1％）与11个（18.6％）（P〈0．05）。脑梗死组〉75％的管腔狭窄数为20例明显高于对照组的3例（，P〈0．05）。结论颈动脉粥样硬化与脑梗死显著相关，颈动脉粥样硬化的程度及斑块的不稳定性是脑梗死的危险因素。     

Carotid atherosclerotic plaque instability in patients with acute myocardial infarction

The instability of atherosclerotic plaque is partly determined by local factors, but systemic factors such as infection, inflammation, autoimmunity or genes might also be important. We aimed to analyze whether patients with acute myocardial infarction (AMI) might have a higher proportion of unstable plaques in the carotid arteries compared with patients who had had no acute coronary events. METHODS: Sixty-nine consecutive patients with AMI (Group 1) and 95 patients without acute coronary events (Group 2) had carotid artery duplex ultrasounds. Carotid atherosclerosis was quantified by number of plaques in the two carotid arteries, intimal media thickening and degree of maximal stenosis. According to their morphology, plaques were divided into stable (fibrocalcific) and unstable (soft and/or not homogeneous). RESULTS: The two groups did not differ as regards age (66+/-8 vs. 68+/-19; p=0.3), female sex (13% vs. 21%; p=0.3), mean number of carotid plaques (2.8+/-1 vs. 2.5+/-2; p=0.2), degree of stenosis (59+/-2% vs. 36+/-1%; p=0.2) or intimal media thickening (1.04+/-0.2 vs. 1.06+/-0.2; p=0.8). However, Group 1 pts more frequently had unstable carotid plaques compared with Group 2 (43% vs. 15%; p=0.004), and had a greater number of unstable carotid plaques (0.51+/-0.6 vs. 0.16+/-0.4: p<0.0001) and a higher ratio of unstable to stable plaque (19% vs. 8%; p=0.005). In the overall population, logistic regression analysis showed that after adjustment for degree of maximal stenosis, the presence of coronary artery event (AMI pts) predicted the presence of unstable carotid plaque (OR: 4.3 95% CI: 2.0-9.2; p=0.0002). CONCLUSION: Patients with unstable coronary artery disease expressed clinically as AMI, frequently had unstable atherosclerotic plaques in other arterial sites such as carotid arteries. This finding supports the hypothesis that plaque instability might reflect a systemic process.     

Predictive factors of coronary lesions in aortic stenosis in adults

The frequent coexistence in adults of a tight aortic stenosis and coronary arterial lesions raises problems of therapeutic and diagnostic approach. In an attempt at selecting indications for coronary arteriography, we studied 253 patients with severe aortic stenosis who were explored by that method. 177 patients (70 p. 100) had no coronary disease (group I); 76 patients (30 p. 100) had significant coronary lesions (group II). Group II patients differed from group I patients in several respects: they were older: 65 +/- 9 years on average as against 61 +/- 9 years (p less than 0.01); there was a greater proportion of men in that group: 76 p. 100 vs 58 p. 100 (p less than 0.01); more patients had a history of myocardial infarction: 7 p. 100 vs 0.5 p. 100 (p less than 0.05); calcifications of the coronary arteries were found in 43 p. 100 of the cases as against 15 p. 100 in group I (p less than 0.001); the transvalvular pressure gradient was lower: 50 +/- 30 mmHg vs 72 +/- 31 mmHg (p less than 0.01). There were no other significant differences in risk factors between the two groups, except for overweight which was greater in group II. Attacks of angina were not statistically more frequent in group II (80 p. 100) than in group I (73 p. 100, N.S.). A multifactorial analysis enabled us to establish a discriminant relation involving the patient's age, sex and history of infarction as well as coronary calcifications.(ABSTRACT TRUNCATED AT 250 WORDS)     

Angiographic progression of coronary artery disease and the development of myocardial infarction

There are few data on angiographic coronary artery anatomy in patients whose coronary artery disease progresses to myocardial infarction. In this retrospective analysis, progression of coronary artery disease between two cardiac catheterization procedures is described in 38 patients: 23 patients (Group I) who had a myocardial infarction between the two studies and 15 patients (Group II) who presented with one or more new total occlusions at the second study without sustaining an intervening infarction. In Group I the median percent stenosis on the initial angiogram of the artery related to the infarct at restudy was significantly less than the median percent stenosis of lesions that subsequently were the site of a new total occlusion in Group II (48 versus 73.5%, p less than 0.05). In the infarct-related artery in Group I, only 5 (22%) of 23 lesions were initially greater than 70%, whereas in Group II, 11 (61%) of 18 lesions that progressed to total occlusion were initially greater than 70% (p less than 0.01). In Group I, patients who developed a Q wave infarction had less severe narrowing at initial angiography in the subsequent infarct-related artery (34%) than did patients who developed a non-Q wave infarction (80%) (p less than 0.05). Univariate and multivariate analysis of angiographic and clinical characteristics present at initial angiography in Group I revealed proximal lesion location as the only significant predictor of evolution of lesions greater than or equal to 50% to infarction. This retrospective study suggests that myocardial infarction frequently develops from previously nonsevere lesions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Repeated coronarographies in 122 medically treated patients

122 patients treated medically 115 men and 7 women aged 51.9 +/- 8.51 years (range 32 to 79 years) underwent repeat coronary angiography 34 +/- 26 months (1 month-11 years) after the initial investigation Patients with normal coronary arteries were excluded. The repeat investigation was performed for aggravation and persistance of symptoms in 74 cases, myocardial infarction in 14 cases, with a view to aortocoronary bypass in 23 cases, for cardiac failure in 8 cases and for ventricular arrhythmias in 3 cases. Three groups of patients could be distinguished: Group I: the coronary angiography was unchanged (41 patients, 33.6 p. 100). The interval between the two investigations was 30.7 +/- 24.8 months. Group II: the coronary lesions had regressed in 12 patients (9.8 p. 100). The interval between the two investigations was 29.4 +/- 23 months. The degree of stenosis was reduced in 6 cases; recanalisation of an occluded artery was demonstrated in 3 cases; coronary spasm was diagnosed in 3 cases. Paradoxically, 4 patients had developed lesions on other coronary segments. Group III: the coronary lesions had progressed in 69 patients (56.6 p. 100). The interval between the two investigations was 36.8 +/- 26.9 months. The progression was observed on a pre-existing stenosis in 51 cases and on an initially normal segment in 34 cases. Left ventricular function had worsened in 21.7 p. 100 of patients compared to only 5.6 p. 100 of patients in groups I and II (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

颈动脉粥样硬化与冠状动脉狭窄程度的关系

探讨颈动脉粥样硬化病变的性质、程度及其与冠状动脉狭窄程度的关系。选择200例冠状动脉造影患者，并经颈动脉DSA及B超检查。根据造影结果分为冠心病组和非冠心病组(对照组)。根据冠状动脉狭窄直径，冠心病组再分成三个亚组。结果发现，颈动脉粥样硬化与冠状动脉狭窄之间呈线性正相关，颈动脉狭窄较冠状动脉狭窄发生率低，但随着冠状动脉狭窄程度加重，颈动脉粥样斑块的发生率明显增加，且颈动脉狭窄亦有加重趋势。结果提示，颈动脉粥样硬化与冠状动脉狭窄密切相关。对中年以上人群，尤其是有多种危险因素者，常规进行颈动脉超声检查，可为早期发现和筛选心脑血管疾病高危患者提供依据。     

Functional significance of coronary collateral perfusion in preserving myocardial integrity

Coronary collateral perfusion to the completely obstructed coronary artery was evaluated by coronary cineangiography in 32 patients. In 13 patients, there was neither history of severe chest pain of longer than 30-min duration nor electrocardiographic evidence of a transmural myocardial infarction (Group I). Among patients undergoing intracoronary thrombolytic therapy for the completely occluded infarct-related coronary artery within 6 h after the onset of symptoms of the first acute myocardial infarction, 19 patients had a history of preinfarction angina (Group II). Collateral visualization (collateral index) was found to be significantly greater in Group I (2.5 +/- 0.5, SD) than in Group II (0.9 +/- 1.0) (p less than 0.01). Group I patients had a longer history of angina (25 +/- 25 months) than did Group II patients (17 +/- 18 months) (p = NS). These findings indicate that well-developed coronary collateral vessels preserve myocardial integrity upon acute coronary occlusion and that a long-standing angina indicative of myocardial ischemia may play an important role in developing collateral channels.     

Totally occluded coronary arteries with normal LV function: clinical and angiographic profile

The clinical and coronary angiographic profile of 50 patients (Group I) with total occlusion of one or more major coronary arteries in the absence of electrocardiographic findings of myocardial infarction and normal segmental and global left ventricular (LV) functions were analysed to identify any variables responsible for this observation. Twenty five age and sex matched patients (Group II), who had 100% occlusion of at least one major coronary artery with significant wall motion abnormalities on LV angiograms, served as controls. The mean duration of angina before angiography or the occurrence of acute coronary event was significantly longer in Group I (2.8 +/- 2.2 yrs) compared to Group II (1.2 +/- 1.2 yrs; p less than .05) patients. RCA was found totally occluded more often in Group I as compared to Group II (60% vs 32%; p less than .05) patients, whereas complete occlusion of LAD occurred more frequently in Group II than in Group I (70% vs 32%; p less than .05). Significant stenoses in other arteries was found in 88% of Group I, compared to 48% of Group II patients (p less than .001). Although there was no significant difference in the frequency of collaterals feeding the totally occluded arteries in the two groups, 80% of patients in Group I had grade 3 collaterals compared to only 30% in Group II patients (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

不稳定型心绞痛患者血清妊娠相关蛋白A与颈动脉粥样硬化的相关性

目的探讨颈动脉粥样硬化、血清妊娠相关性蛋白A与不稳定型心绞痛、稳定型心绞痛、非冠心病的相关性。方法因胸痛入院的患者1 w内行冠脉造影,排除急性及亚急性心梗后,不稳定型心绞痛、稳定型心绞痛、非冠心病各40例被纳入研究中,进行冠状动脉Gensini评分;彩超检测颈动脉内中膜厚度、斑块形成情况,应用酶联免疫吸附法测定血清妊娠相关蛋白A水平,并进行统计学分析。结果除吸烟史外,各组间其余基线资料匹配;不稳定型心绞痛、稳定型心绞痛的冠脉Gensini评分、颈动脉粥样硬化指标均较非冠心病高(P<0.001);不稳定型心绞痛组比稳定型心绞痛及非冠心病组血清妊娠相关蛋白A的浓度高(P<0.001),妊娠相关蛋白A在不稳定型心绞痛患者明显升高,其与颈动脉粥样硬化指标、冠脉Gensini积分正相关;Crouse积分预测心绞痛型冠心病,敏感度、特异度分别为0.79、0.92;颈动脉内中膜厚度平均值预测心绞痛型冠心病敏感度、特异度分别为0.97、0.85;妊娠相关蛋白A预测不稳定型心绞痛敏感度、特异度分别为0.825、0.937。结论颈动脉粥样硬化指标与冠状动脉Gensini积分有较好的相关性,而妊娠相关蛋白A可作为预测不稳定型心绞痛的指标;二者联合检测可能是预测不稳定型心绞痛的重要临床依据。     

Patency of the artery responsible for myocardial infarction: role on ventricular function and long-term outcome]

Out of 3,171 consecutive patients referred for coronary angiography, 240 were selected on the following criteria: recent primary myocardial infarction, single vessel coronary disease, no angioplasty or coronary surgery after the angiography which was performed 20 to 90 days after the onset of myocardial infarction. The patients were divided into 2 groups according to whether the artery responsible for infarction was patent (Group I: 115 patients) or not (Group II: 125 patients). The left ventricular ejection fraction was significantly higher in Group I (58 +/- 10.8%) than in Group II (53.7 +/- 11.3%) and end systolic and end diastolic left ventricular volumes were greater in Group II (51.8 +/- 22 ml/m2 and 88 +/- 22 ml/m2 respectively). Long-term follow-up (56 +/- 25 months in Group I and 61 +/- 26 months in Group II) was possible in 112 patients in Group I and 123 patients in Group II. Of the 7 patients who died in group II, 4 deaths were of cardiac origin; in addition, 2 cases of sustained ventricular tachycardia were observed in this group. None of the 6 deaths observed in Group I was of cardiac origin and there were no cases of ventricular tachycardia (p = 0.05). The functional status was identical in the two groups at the end of the study. These results suggest that the patency of the coronary artery responsible for myocardial infarction at a distance from the acute event is associated with better left ventricular function and a better long term prognosis.     

Influence factors on coronary collateral development

In order to evaluate the influence factors on coronary collateral development, we compared various factors between two groups. Group I consisted of the 69 patients performed coronary angiography within 6 hours after the onset of acute myocardial infarction (MI) and Group II consisted of the 56 patients without MI because having good collaterals nevertheless whose one coronary artery was totally occluded or had a 99% stenosis. Group I (24/69, 35%) had a higher frequency of Diabetes mellitus than Group II (11/56, 20%) and had a lower frequency (30/69, 43%) of multivessel disease than Group II (39/56, 70%). The patients having angina duration more than 6 months were more in Group II (37/56, 60%) than in Group I (18/69, 26%). No significant differences existed between these two groups in age, smoke, hyperlipidemia and hypertension. In conclusions, the patients with good collateral have high frequency of multivessel disease and long history of angina pectoris. Diabetes mellitus is a inhibit factor on coronary collateral development.     

The role of carotid atherosclerosis in the distinction between ischaemic and non-ischaemic cardiomyopathy.

AIM: Sometimes ischaemic cardiomyopathy is a result of severe coronary artery disease of an occult course, without typical symptoms or evidence of myocardial infarction. This form of presentation is usually indistinguishable from non-ischaemic dilated cardiomyopathy. Carotid bifurcation atherosclerosis and coronary artery disease have been shown to be strongly associated. We prospectively examined the value of extracranial carotid atherosclerosis in the distinction between ischaemic and non-ischaemic aetiology in patients with clinically unexplained cardiomyopathy. METHODS AND RESULTS: Seventy-eight patients with undetermined dilatation and diffuse impairment of the left ventricular contraction were studied within 28 months. They underwent carotid scan and coronary arteriography. Carotid atherosclerosis was found to be very common in ischaemic and rare in non-ischaemic cardiomyopathy. The presence of at least one abnormal carotid finding (intima-media thickness >1 mm, plaques, severe carotid stenosis) was 96% sensitive and 89% specific for ischaemic cardiomyopathy. CONCLUSION: Carotid scanning may be a useful screening and decision making tool in patients with cardiomyopathy of indecisive cause. Patients with carotid atherosclerosis are likely to suffer from severe coronary artery disease. Coronary angiography and subsequent myocardial viability studies, when indicated, could be considered early during their evaluation. In contrast, a negative carotid scan predicts non-ischaemic cardiomyopathy.     

The comparison between self-expanding and balloon expandable stent results in left anterior descending artery

The first Wallstent results had high thrombosis and death. It was reported that the left anterior descending (LAD) artery was the vessel implicated in major complications that occurred in patients who received a Wallstent. Subsequently, Wallstent applications were refrained from with LAD lesions. However, the promising results of second-generation self-expanding Magic Wallstent implantation have been reported recently. The purpose of this study is to assess the immediate and intermediate clinical outcomes of patients undergoing self-expanding Magic Wallstent implantation at the LAD site and to compare those outcomes with those of a similar group of patients undergoing balloon expandable stenting at the same site. Between 1995 and 1999, 255 consecutive patients underwent LAD stenting at our center. The study population was divided into two groups based on the mode of delivery (self-expanding versus balloon-expandable) of stent design. Group I included 97 patients in whom self-expanding Magic Wallstents were implanted. Group II included 158 patients in whom various types of balloon-expandable stents were implanted. Procedural success was defined as successful deployment of the stent in the absence of adverse cardiac events (death, acute myocardial infarction, emergency coronary bypass surgery). Clinical success was defined as the absence of adverse cardiac events (death, acute myocardial infarction, emergency coronary bypass surgery, repeat balloon angioplasty) within the first two weeks. The mean follow-up period was 8 ± 5.3 months for Group I and 9.8 ± 7.5 months for Group II. There was no difference in baseline characteristics between the two groups. Fourteen patients in Group I and 22 patients in Group II had bailout procedures. The number of patients with reference vessel diameter less than 3 mm was 37 in Group I and 60 in Group II. The stent length was greater in Group I than in Group II (p=0.0003). In Group I, stenting improved minimal lumen diameter (MLD) from 0.65 ± 0.4 mm to 2.35 ± 0.4 and percent diameter stenosis (PDS) from 76.24 ± 17.3 to 22.78 ± 13.6. In Group II, stenting improved MLD from 0.73 ± 0.4 mm to 2.49 ± 0.5 and PDS from 76.71 ± 15.5 to 18.99 ± 9.6. Final MLD and final PDS improved more in Group II than Group I. Stent could not be delivered in three patients in Group I and nine in Group II. In Group II, six stents were dislocated from its delivery system. Procedural and clinical success and subacute stent thrombosis rates were 93.8%, 85.6%, and 7.2% in Group I, and 93%, 86.7%, and 5.1% in Group II, respectively. Within the first two weeks, death occurred in one patient in each group, acute myocardial infarction in four (Group I) and two (Group II) patients; coronary bypass surgery in three (Group I) and five (Group II) patients, and balloon angioplasty in two (Group I) and four (Group II) patients, respectively. In Group I, following the first two weeks, no patients died, two patients had nonfatal myocardial infarction, and coronary bypass surgery and target vessel repeat balloon angioplasty was required in five and ten patients, respectively. In Group II, one patient died in the follow-up period, there was no nonfatal myocardial infarction, and bypass surgery and target vessel repeat balloon angioplasties were required in three and eleven patients, respectively. None of these differences in clinical events was statically significant. We found that self-expanding Magic Wallstent implantation can be performed in LAD lesions and was associated with a rate of early clinical results and intermediate term clinical results similar to that of balloon-expandable stents in LAD arteries. In conclusion, the Magic Wallstent may confidently be used for LAD lesions.     

Effects of severity of the residual stenosis of the infarct-related coronary artery on left ventricular dilation and function after acute myocardial infarction.

OBJECTIVES. This study was designed to evaluate the relation between the severity of the residual stenosis of the infarct-related artery and changes in left ventricular volume and function after a first anterior myocardial infarction. BACKGROUND. Although thrombolytic therapy improves clinical outcome after acute myocardial infarction, the relations between the severity of the residual stenosis of the infarct-related artery and postinfarction left ventricular remodeling and function are unclear. METHODS. Fifty-eight patients with a first anterior myocardial infarction and significant disease only in the left anterior descending coronary artery on arteriography performed after 7 to 10 days were evaluated. All patients received thrombolytic therapy. Residual stenosis of the infarct-related artery was measured with quantitative coronary arteriography. Left ventricular volumes and ejection fraction were measured by echocardiography and radionuclide angiography, respectively, 7 to 10 days, 6 months and 1 year after infarction. End-diastolic and end-systolic left ventricular volumes were measured by two-dimensional echocardiography and normalized to body surface area. Patients were classified into three groups according to baseline residual stenosis severity: total occlusion (Group I), minimal lesion diameter less than 1.5 mm (Group II) and minimal diameter greater than or equal to 1.5 mm (Group III). RESULTS. Group I patients had significantly greater left ventricular end-diastolic and end-systolic volumes at 6 months and 1 year than did the other groups. Group II patients had greater end-diastolic and end-systolic volumes than did Group III patients at 1 year. In addition, Group I patients had a lower ejection fraction at 1 year than that of the other groups. The minimal lesion diameter was significantly correlated with percent change in end-diastolic volume at 1 year. CONCLUSIONS. The severity of the baseline residual stenosis of the infarct-related artery is an important predictor of change in left ventricular volumes in the 1st year after infarction. Total occlusion of the infarct-related artery is associated with greater left ventricular dilation and functional impairment.     

Long-term results of thrombolytic therapy with and without percutaneous transluminal coronary angioplasty

The effects of combined intravenous and intracoronary streptokinase without (Group I, n = 103) or with (Group II, n = 103) immediate coronary angioplasty were evaluated during a long-term (3 year) follow-up of 206 patients with acute transmural myocardial infarction. There were no baseline differences between the groups with regard to gender, age, infarct location, serum creatine kinase levels, time between onset of symptoms and treatment and coronary artery patency rate. Angioplasty was performed with a success rate of 69% and a reocclusion rate of 2%. Elective angioplasty was performed in 22 (21%) of 103 patients in Group I and 9 (9%) of 103 patients in Group II, with a success rate of 86% and 100%, respectively, reflecting the higher incidence of angina pectoris and antianginal therapy in Group I. Coronary bypass surgery was performed in 21 (20%) of 103 patients in Group I and 20 (19%) of 103 patients in Group II; there was one operative death in each group. During follow-up, coronary reocclusion or reinfarction, or both, occurred in 25 (29%) of 87 patients in Group I and in 16 (18%) of 87 patients in Group II with reperfused vessels (p = NS). Heart failure occurred in 40% of the patients in both groups who had increased end-diastolic and end-systolic volumes. The survival rate after 3 years was 78% in Group I and 80% in Group II (p = NS). Thus, long-term follow-up of patients with acute transmural infarction treated with and without immediate angioplasty does not demonstrate any difference with regard to clinical outcome and mortality.     

An ultrasonic study of the relationship between extracranial carotid atherosclerosis and ischemic cerebrovascular disease in Japanese]

The study is to evaluate the relationship between extracranial carotid atherosclerosis and ischemic cerebrovascular disease using noninvasive B-mode ultrasonography and X-ray computed tomography. The sensitivity of bruits for diagnosing severe carotid stenosis was also evaluated. A total of 229 consecutive Japanese patients were recruited for this study, of which 97 had chronic-stage ischemic cerebrovascular disease and remaining 132 patients had at least one risk factor for atherosclerosis. Carotid atherosclerosis was evaluated by B-mode ultrasonography. Ischemic cerebrovascular disease was assessed by history taking, neurological findings and X-ray CT examination. The severity of carotid atherosclerosis was assessed by using two indices; plaque score and maximum percentage diameter stenosis. We also evaluated whether it was ulcerated plaque or not. Plaque score was computed by summing up all carotid plaque thicknesses (mm) on both sides. According to the CT findings, cerebral infarction was divided into two types; deep subcortical infarction and cortical infarction. The incidence of cerebral infarction increased in relation to plaque score and maximum percentage stenosis. Although the incidence of cerebral infarction in patients without carotid atherosclerosis was only 33% (38/116), it in patients with moderate carotid atherosclerosis (plaque score > 5) was 59% (26/44) (p < 0.05, chi-square test). The incidence of ipsilateral infarction was revealed to be higher in patients with severe (50% or more) carotid stenosis (61%) than in cases of mild stenosis (28%) (p < 0.05). Thirteen patients had ulcerated plaques and they suffered more frequently cerebral infarction than patients without ulcerated lesions. Cortical infarction was more frequent in patients with severe carotid stenosis than in patients without carotid atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)