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J Am Coll Cardiol, 2006; 47:2413-2419, doi:10.1016/j.jacc.2005.11.091
© 2006 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: STUDY WITH INTRAVASCULAR ULTRASOUND

Negative Remodeling and Calcified Plaque in Octogenarians With Acute Myocardial Infarction

An Intravascular Ultrasound Analysis

Salah-Eddine Hassani, MD*, Gary S. Mintz, MD{dagger}, Helen S. Fong, BA*, Sang-Wook Kim, MD*, Zhenyi Xue, MS*, Augusto D. Pichard, MD*, Lowell F. Satler, MD*, Kenneth M. Kent, MD, PhD*, William O. Suddath, MD*, Ron Waksman, MD* and Neil J. Weissman, MD*,*

* Cardiovascular Research Institute/Medstar Research Institute, Washington Hospital Center, Washington, DC
{dagger} Cardiovascular Research Foundation, New York, New York

Manuscript received August 8, 2005; revised manuscript received November 22, 2005, accepted November 28, 2005.

* Reprint requests and correspondence: Dr. Neil J. Weissman, Washington Hospital Center, 100 Irving Street, NW, Suite EB 5123, Washington, DC 20010. (Email: Neil.J.Weissman{at}medstar.net).


   Abstract
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 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES: The goal of this study was to use intravascular ultrasound (IVUS) to compare octogenarians versus patients <65 years of age with regard to culprit lesion morphology in acute myocardial infarction (MI).

BACKGROUND: Although octogenarians represent the fastest-growing segment of our population and have a higher risk profile, they are underrepresented in therapeutic trials.

METHODS: Between 2002 and 2005, 42 octogenarians and 52 patients <65 years of age underwent pre-intervention IVUS within 2 days from onset of an MI. Qualitative and quantitative measurements were performed at the lesion site and at the proximal and distal references. Positive remodeling was defined as a remodeling index (lesion/mean reference arterial area) ≥1.

RESULTS: Elderly patients mostly (71%) presented with non–ST-segment elevation myocardial infarction (NSTEMI), whereas patients <65 years of age presented almost equally with ST-segment elevation myocardial infarction (STEMI) and NSTEMI (56% vs. 44%). The frequency of rupture/dissection was greater in the <65-year-old group (32% vs. 9%, p = 0.009), and culprit lesions contained more thrombus in this group (14% vs. 2%, p = 0.04). Conversely, in octogenarians, lesions were predominantly calcified (57% vs. 10%, p < 0.001) and longer (20.9 ± 7.8 mm vs. 16.6 ± 6.1 mm, p = 0.004) with less positive remodeling (19% vs. 56%, p < 0.001). On multivariant logistic regression analysis, age was the only independent predictor of calcified plaque (p = 0.02) and remodeling (p = 0.005).

CONCLUSIONS: Negative remodeling and calcified plaque with rare plaque ruptured were common in elderly people with acute MI. These findings may contribute to the difference in clinical presentation and may suggest a different pathophysiologic mechanism of MI in octogenarians.

Abbreviations and Acronyms
  CSA = cross-sectional area
  EEM = external elastic membrane
  IVUS = intravascular ultrasound
  MI = myocardial infarction
  NSTEMI = non–ST-segment elevation myocardial infarction
  P&M = plaque and media
  STEMI = ST-segment elevation myocardial infarction

Multicenter clinical trials of revascularization have routinely underrepresented elderly patients compared with their prevalence in clinical practice. As a result, the literature has been composed mostly of retrospective single-institution experiences with small numbers of patients. Nonetheless, studies of elderly patients have consistently reported a lower rate of successful revascularization and more adverse outcomes in octogenarians presenting with an acute myocardial infarction (MI). The reasons for these adverse findings are not well understood. As octogenarians are becoming a more common group of patients in clinical practice, it is important to understand how their coronary artery disease may differ from that of younger patients. The purpose of the present study was to use intravascular ultrasound (IVUS) to study culprit lesions in octogenarians presenting with an acute MI and to compare these findings with those from a cohort of younger patients (<65 years old).


   Methods
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Patient population.   Between 2002 and 2005, approximately 1,400 patients were admitted for acute MI to the Washington Hospital Center: 945 (67%) with non–ST-segment elevation myocardial infarction (NSTEMI) and 455 (33%) with an ST-segment elevation myocardial infarction (STEMI). During this period, there were 189 octogenarians, of whom 134 (71%) had NSTEMI and 55 (29%) had STEMI. Conversely, of 739 patients <65 years of age, 469 (63%) had NSTEMI and 270 (37%) had STEMI. Of these, a total of 42 octogenarians and 52 patients <65 years of age underwent pre-intervention IVUS within two days from symptom onset; these two representative groups of patients constitute the cohorts for the present study.

The presence of STEMI was determined by >30 min of continuous chest pain, a new ST-segment elevation ≥2 mm on at least two contiguous electrocardiographic leads, and creatinine kinase-MB >3 times normal. The presence of NSTEMI was diagnosed by chest pain and a positive cardiac biochemical marker without new ST-segment elevation. Risk factors and previous cardiovascular disease were reviewed via retrospective chart review. Hyperlipidemia was defined as receiving lipid-lowering therapy or total cholesterol >5 mmol/l or serum triglycerides >2 mmol/l. Hypertension was defined as receiving medication to lower blood pressure or known blood pressure values of ≥140 mm Hg systolic or ≥90 mm Hg diastolic on two or more occasions. Chronic renal failure was defined as a baseline serum creatinine value ≥1.8 mg/dl. The vessel with the culprit lesion was determined based on a combination of electrocardiogram findings, left ventricular wall motion abnormalities (left ventriculography or echocardiography), and angiographic lesion morphology. We excluded patients with prior coronary artery bypass failure, stent thrombosis, or restenosis after percutaneous coronary intervention.

Angiographic analysis.   Culprit lesion location was designated as proximal, mid, or distal. Calcification was identified as readily apparent radio-opacities within the vascular wall. Angiographic thrombus was defined as a filling defect seen in multiple projections surrounded by contrast in the absence of calcification. All angiograms were analyzed independently with an automated edge-detection algorithm (CAAS II system, Pie Medical, Maastricht, the Netherlands) using standard protocols (1). With the external diameter of the contrast-filled catheter as the calibration standard, the minimal lumen diameter and reference-segment lumen diameter at end diastole before intervention was measured from orthogonal projections and the result from the "worst" view were recorded.

IVUS imaging protocol.   All IVUS studies were performed before any intervention and after intracoronary administration of 100 to 200 µg nitroglycerin. The IVUS imaging was performed with a 30- or 40-MHz mechanical scanning IVUS catheter (Boston Scientific Corporation/SCIMED, Maple Grove, Minnesota) in 88 cases or a 20-MHz electronic scanning IVUS (Volcano, Rancho Cordova, California) in 4 cases. The IVUS catheter was advanced distal to the lesion, and retrograde imaging was performed back to the aorta-ostial junction (with a motorized pullback). The IVUS imaging was recorded only during transducer pullback onto high-resolution S-VHS videotape for offline analysis.

IVUS analysis.   Qualitative analysis was performed according to criteria of the American College of Cardiology clinical expert consensus (2). Calcium was brighter than the adventitia with acoustic shadowing. The location (superficial vs. deep) was noted, and the arc (in degrees) and length (in millimeters) were measured. Hyperechoic plaque was as bright as or brighter than the adventitia without shadowing, and hypoechoic plaque was less bright than the adventitia. The identification of thrombus required at least two of the following: distinct hypoechoic mass, brightly speckled plaque, channeling within the plaque, evacuated plaque cavity, or detached mobile mass. A ruptured plaque contained a cavity that communicated with the lumen with an overlying residual fibrous cap fragment. A dissection was a longitudinal tear in the plaque parallel to the vessel wall.

Using planimetry software (TapeMeasure, INDEC Systems Inc., Mountain View, California), the lesion and references were analyzed as follows: external elastic membrane (EEM) cross-sectional area (CSA) (mm2), lumen CSA (mm2) and plaque and media (P&M) CSA (mm2). Plaque burden (%) was calculated as P&M divided by EEM CSA. Area of stenosis was calculated as the mean reference lumen minus lesion lumen CSA divided by the mean reference lumen CSA. Remodeling index was defined as the lesion EEM divided by the mean reference EEM CSA. Positive remodeling was defined as a remodeling index ≥1.

Statistical analysis.   Statistical analysis was performed using the Statistical Analysis System version 8.2 (SAS Institute Inc., Cary, North Carolina). Data are expressed as mean ± SD for continuous variables and as percentages for categorical variables. The Student t test was used to compare continuous variables, and the chi-square test or the Fisher exact test was used to compare categorical variables. If the expected number of counts was <5, a Fisher exact test was performed for the categorical variables. We conducted multivariate logistic regression analysis to identify independent predictors of clinical presentation and plaque morphology. Variables entered into the multivariant model were determined from a univariant analysis with any parameter meeting a p ≤ 0.20. Overall, a value of p < 0.05 was considered as significant.


   Results
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Discussion
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Clinical findings.   Patient characteristics are presented in Table 1. There was no significant difference in gender and race between the two patient age groups. There was more obesity in the younger (<65-year-old) age group, whereas octogenarians had more peripheral vascular disease and chronic renal insufficiency. Serum enzyme, white blood cell, and hemoglobin levels were greater in the younger age group, whereas thrombolysis was used less commonly in the older group. Triglycerides were higher and there was a trend for a higher cholesterol level in the younger group. Left ventricular ejection fraction was lower in the older patient group, with a trend for more heart failure. Older patients predominately (71%) presented with NSTEMI. Younger patients had less aspirin or statin use at admission. No significant difference was found in stent use and anticoagulation use between the two groups. However, there was a trend for a longer length of hospital stay in octogenarians.


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  		Table 1. Patient Characteristics
 
Angiographic characteristics.   Octogenarians had more multivessel disease (79% vs. 40%, p < 0.05). Culprit lesion locations were statistically similar between the two groups; in half of the cases, the culprit lesion was found in the mid left anterior descending coronary artery. Angiographic analysis is shown in Table 2. The presence of angiographic thrombus was more common and calcifications were less common in the younger group of patients. Lesions were longer and less narrowed in older patients.


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  		Table 2. Angiographic Analysis
 
IVUS findings.   Plaque composition was significantly different between the two groups (Table 3). Lesions were more often hypoechoic (50% vs. 19%, p = 0.001) and noncalcific (20% vs. 4%, p = 0.03) with more thrombi and ruptured/dissected plaques in patients <65 years of age (Fig. 1). Calcified plaques were more common (57% vs. 10%, p < 0.001) and the amount of calcium was greater in older patients (Fig. 2). Aspirin or statin use at the time of admission was not a predictive factor of plaque morphology or clinical presentation in the two age groups.


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  		Table 3. Qualitative Intravascular Ultrasound Findings
 

Figure 1
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  		Figure 1 Soft plaque and ruptured cavity in a patient <65 years old with acute myocardial infarction. EEM = external elastic membrane.

 

Figure 2
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  		Figure 2 Negative remodeling and calcified plaque in an octogenarian with acute myocardial infarction. EEM = external elastic membrane.

 
As shown in Table 4, culprit lesions were shorter and more often presented with positive remodeling (56% vs. 19%, p < 0.001) in younger patients. In concordance with longer lesions, proximal and distal reference segment plaque burden was greater in older patients. Multiple plaque ruptures were not found in any octogenarian.


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  		Table 4. Quantitative Intravascular Ultrasound Findings
 
Predictors of clinical presentation and plaque morphology.   Because of the imbalance in frequency of STEMI versus NSTEMI in the two age groups, we sought to determine which clinical, angiographic, and IVUS factors were caused by age and which by STEMI status. Using multivariate logistic regression analysis with STEMI as the outcome, independent predictors of the differences between STEMI and NSTEMI were smoking (p = 0.004), peak troponin (p = 0.005), and calcified plaque (p = 0.01). Because calcified plaque was related to both age and STEMI, multivariate logistic regression analysis using calcified plaque as the outcome was also performed to determine whether the calcification is attributable to age or to STEMI. Age was the only independent predictor of calcified plaque (p = 0.02). In addition, age was a predictor of negative remodeling (p = 0.005).


   Discussion
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 Abstract
 Methods
 Results
 Discussion
References
 
The present study showed that culprit plaques in MI are distinct between octogenarians and patients <65 years of age. Octogenarians have longer lesions, more reference segment disease, more calcified plaques, and more negative remodeling, whereas younger patients, as previously reported in several studies, have ruptured hypoechoic plaques with positive remodeling. Age may be related to the differences in plaque morphology, which could account for the ascribed frequencies of STEMI versus NSTEMI in the two age groups.

Patient characteristics and clinical presentation.   Elderly people had more extensive cardiac and noncardiac disease with more risk factors, including known coronary artery disease, peripheral disease, chronic renal failure, heart failure, low ejection fraction, multivessel disease, and anemia. Our findings are consistent with those from previous studies reporting more comorbidities in octogenarians (3–8).

Similar to other reports (9–12), STEMI was more frequent in younger patients, whereas NSTEMI was more frequent in older patients. The pathophysiologic alterations of coronary arteries (dilation, tortuosity, and endothelial dysfunction) and apoptosis of vascular smooth cells with aging (13) may explain the differences in plaque morphology with more calcified plaque and diffuse lesions (larger reference segment plaque burden) in octogenarians, although proof of this hypothesis would require further investigation. Using cardiovascular magnetic resonance, Moon et al. (14) have reported that the distinction between STEMI/NSTEMI is mainly the difference in infarct size, whereas Kloner et al. (15) have shown greater ischemic preconditioning in the older heart with acute MI. The higher prevalence of female gender, comorbidities, and chronic treatment with aspirin and/or statins may also contribute to the higher frequency of NSTEMI (16–20). Using multivariate logistic regression analysis, calcified plaque was a predictive factor of the clinical presentation in our study. None of these previous studies had assessed or explained the underlying differences in STEMI/NSTEMI plaque morphology.

Angiographic and IVUS findings.   Culprit plaques in octogenarians were more calcified and longer with more negative remodeling and larger reference plaque burden, but less plaque rupture and thrombi formation. To our knowledge, this is the first study that suggests a different pathophysiologic mechanism in elderly people with MI that would potentially explain the higher frequency of NSTEMI in this age group.

Several reports have shown that in MI lesions, positive remodeling is observed in 30% to 80% and hypoechoic plaque is seen in 30% to 60% of culprit lesions (21–29).

Some pathologic studies in the past have shown that the pathology of both types of infarct is identical, whereas Phibbs et al. (30) suggested that there is no meaningful pathophysiological distinction between STEMI and NSTEMI. In contrast, Furman et al. (19) suggested distinctive pathophysiologic differences between the two entities because of risk factor changes during the study period.

This study confirms previous reports that calcified plaque and intermediate or negative remodeling are more common in older patients (31–33). Usually, these findings were in stable plaques. However, Gyongyosi et al. (34) have shown that older age is a predictor for constrictive remodeling in patients with unstable angina. It has also been reported that plaque erosion causes thrombus formation and MI and that plaque erosion is associated with negative remodeling (33–35). The lack of ruptured plaque and the dysfunction endothelial caused by the reduced endothelial progenitor cells and the higher homocysteine levels with aging supposes that the plaque erosion may be the main causal mechanism of MI (i.e., NSTEMI) in octogenarians (16,17,36,37). Recently, Hayashi et al. (38) have reported by IVUS and angioscopy in acute MI that patients with plaque erosion have more previous preinfarction angina, less Q-wave MI, and smaller infarction compared with patients with ruptured plaque. The investigators suggested that eroded plaques have less potent thrombogenicity than do ruptured plaques.

Our study also suggests that calcified plaques are not necessarily synonymous with stable plaque, especially in elderly patients. However, calcified plaques in MI may rupture less often or have smaller prerupture necrotic cores and thrombus formation than larger lipid cores in younger patients, resulting in smaller infarct size (i.e., NSTEMI). The calcified plaques seen in octogenarians have been the result of "old" plaque ruptures that healed, leading to a complex heterogeneic morphology. The different pathophysiologic mechanism of MI in elderly people may in part be caused by the plaque morphology (calcified plaque and negative remodeling), which may explain the higher frequency of NSTEMI.

Study limitations.   This study was retrospective. Because of the requirement for pre-interventional IVUS for inclusion in this study, the number of patients is small and constitutes only a small percentage of patients presenting to our institution with an MI during this time period. Thus, some selection bias cannot be excluded entirely. Finally, the insertion of an IVUS catheter through a tight stenosis could have caused changes in lesion geometry that may have contributed to the findings.

Conclusions.   Negative remodeling and calcified plaques were found in octogenarians’ culprit MI lesions. Ruptured plaques were rare in this older population. These morphology findings may contribute to the high frequency of NSTEMI in this population. Therefore, the pathophysiologic mechanism of the MI event is probably different in octogenarians compared with younger patients.


   References
Top
 Abstract
 Methods
 Results
 Discussion
 References
 

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