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Psychosomatics 47:231-239, June 2006
doi: 10.1176/appi.psy.47.3.231
© 2006 Academy of Psychosomatic Medicine
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Symptoms of Posttraumatic Stress Disorder in Patients Who Have Had a Myocardial Infarction

Eyal Shemesh, M.D., Maya Koren-Michowitz, M.D., Rachel Yehuda, Ph.D., Olga Milo-Cotter, M.D., Elmer Murdock, B.S., Zvi Vered, M.D., FACC, Benjamin L. Shneider, M.D., Jack M. Gorman, M.D., and Gad Cotter, M.D., FACC

Received October 15, 2004; revised January 21, June 20, 2005; accepted August 9, 2005. From the Depts. of Psychiatry and Pediatrics, Mount Sinai Medical Center, NY; the Hematology Institute and the Dept. of Cardiology, Assaf-Harofeh Medical Center, Zerifin, Sackler Faculty of Medicine, Tel Aviv Univ., Israel; and Duke University Medical Center, Durham, NC. Address correspondence and reprint requests to Dr. Shemesh, Mount Sinai Medical Center, Box 1230, 1 Gustave L. Levy Place, New York, NY 10029. e-mail: eyal.shemesh{at}mssm.edu


  ABSTRACT

 
TOP
 ABSTRACT
INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
Symptoms of posttraumatic stress disorder (PTSD) and risk factors for recurrent ischemia were evaluated in 65 survivors of a myocardial infarction (MI) at baseline and 6 months afterward. PTSD patients had more uncontrolled cardiovascular risk factors at baseline. Patients with PTSD (N=14) were offered trauma-focused cognitive-behavior treatment (CBT) plus a nonspecific intervention to improve adherence to medical recommendations. Adherence to aspirin improved in recipients of the nonspecific intervention (N=8); PTSD symptoms and cardiovascular risk improved in patients who received CBT (N=6). PTSD may be a treatable risk factor for poor post-MI outcome. Further research is needed to evaluate treatment options.

Key Words: Cardiology • Posttraumatic Stress Disorder

  INTRODUCTION

 
TOP
 ABSTRACT
 INTRODUCTION
METHOD
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
Ischemic heart disease (IHD) is one of the western world's most prevalent health problems. The American Heart Association developed a set of recommendations for secondary prevention of recurrent ischemic episodes in patients who have had a myocardial infarction (MI).1 However, in the recently published international GRACE registry, the 6-month mortality post-MI was approximately 5%, and readmission for severe cardiovascular events was 20%.2 Therefore, the identification of new ways to improve post-MI outcome is still as important in cardiovascular research as it has ever been.

Psychiatric morbidity is increasingly being recognized as an important risk factor for poor post-MI outcome. Therefore, treatment of psychiatric morbidity could be an important way to improve the medical outcome of MI survivors. To date, the best studied post-MI psychiatric morbidity is depression,3–8 but treatment of post-MI depression has led to mixed results.9,10 Depression after MI is frequently comorbid with anxiety symptoms, and a recent large study found that co-occurring anxiety symptoms were primarily responsible for the observed association between depressive symptoms and poor cardiovascular outcome.11

We have previously suggested12 that one factor possibly differentiating post-MI patients with depressive symptoms from patients who are depressed but did not have an MI is the psychological impact of the experience of the MI in and of itself. A myocardial infarction may be emotionally traumatic, and, indeed, approximately 10%–20% of patients report substantial symptoms of the anxiety disorder termed PTSD (posttraumatic stress disorder) after the MI.12–18

MI survivors with PTSD symptoms may view medical recommendations as "traumatic reminders."12,18 In other words, every time an MI survivor takes a medication, it reminds him or her of the illness. If this memory is traumatic, the survivor will strive to avoid it—in the same way that a traumatized war veteran avoids going back to the battlefield, even long after the battle is over. Therefore, PTSD symptoms may worsen medical outcome by decreasing adherence to post-MI medication regimens and other recommendations. In previous studies, we found that PTSD symptoms are associated with non-adherence to aspirin,18 non-adherence to captopril,12 and increased likelihood of cardiovascular readmissions post-MI.18 Other investigators have reported that PTSD symptoms are associated with poor outcome after a heart transplant.19 Because PTSD is associated with poor adherence to medical recommendations, it is possible that it is also associated with increased post-MI cardiovascular risk. If this is the case, treatment of PTSD may be a way to improve cardiovascular risk factor control in affected patients.

After our earlier studies,12,18,20 we recruited a new cohort of MI survivors, aiming to determine whether there is an association between substantial PTSD symptoms and the existence of poorly controlled medical risk factors for recurrent ischemic events. There are highly effective psychotherapeutic (cognitive-behavioral [CBT]) treatments for PTSD, but they have not been studied in patients with cardiovascular illnesses. After they were told that treatment is still experimental at this stage, all patients who were identified in this study as potentially suffering from PTSD were offered the option of psychiatric assessment and treatment. Furthermore, because we already knew that PTSD is associated with non-adherence to treatment recommendations,12,18 we also offered a short adherence-enhancing intervention to all PTSD patients. The study was not designed to evaluate treatment effects, and there was no random allocation to treatment. However, we present follow-up information for patients who were treated with either modality, compared with those who were not treated, to further explore the relationship between PTSD symptoms and poor risk-factor control post-MI.


  METHOD

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
Patients and Procedure
One hundred consecutive patients who had had their first MI were asked to come for a clinic visit 6–9 months after the MI. MI was diagnosed in all patients by the treating physicians, on the basis of symptoms, ECG changes, and enzyme changes, according to the criteria endorsed by the American College of Cardiology/European Society of Cardiology.21 In each case, the diagnosis of MI was verified by the study cardiologist before enrollment. Sixty-five patients who came to the visit and consented to the study were evaluated for the presence of cardiovascular risk factors (see below). They were asked to answer a short, validated self-report PTSD questionnaire, the Impact of Event Scale (IES).22 Patients who met the threshold PTSD criterion on this scale were offered a more thorough psychiatric assessment and, if they wished, treatment. All patients were reassessed 6 months after the initial evaluation. The study was approved by the Institutional Review Board and involved a full, written-consent procedure.

Risk-Factor Profile
We evaluated the existence of medical risk factors for recurrent ischemic events, based on published recommendations by the American Heart Association.1 We counted only existing risk factors (such as high blood pressure, high cholesterol), following the general approach recommended by the American Heart Association in computing a cardiovascular risk profile.23 The existence of a risk factor means, in this scheme, that it was poorly controlled by the patient's current treatment; these risks would be expected to be present more often in non-adherent patients:

  1. High blood pressure, despite treatment aimed at lowering blood pressure. (High, or "uncontrolled" blood pressure "score: 1" was defined as three consecutive measurements showing a value of either >140 systolic or >90 diastolic)
  2. High LDL cholesterol blood levels, despite treatment aimed at lowering cholesterol. (LDL cholesterol fasting levels of 100 mg% or more were considered high "score: 1"
  3. Obesity. (Obesity [score: 1] was defined as Body Mass Index [BMI] that is higher than 30 kg/m2 in patients who received dietary counseling)
  4. Smoking. (Self-reported smoking in a face-to-face interview with a study nurse [score: 1] in patients who were counseled to stop smoking)
  5. Adherence to aspirin treatment. (Patients were considered adherent [score: 0] if their platelet thromboxane-generation tests show a level that is consistent with impaired generation [positive aspirin effect]). A detailed description of the method used to define aspirin adherence is presented below.
  6. Diabetes mellitus. (Hemoglobin A1C was evaluated in patients with known diabetes mellitus. Values of HgA1C ≥7.0 g% were considered as uncontrolled diabetes in patients who were under treatment for diabetes)

This method yields a score of 0–6 for each patient, corresponding to the number of uncontrolled risk factors. Although we treated the risk factors as dichotomies (Yes/No presence of a risk factor), in secondary analyses, we also compared some of them as continuous variables. Thus, in secondary analyses, we looked individually at mean arterial pressure (MAP), LDL cholesterol, BMI, and platelet thromboxane production.

Assessment of Adherence by Use of Thromboxane-Generation Tests
Aspirin, an anticoagulant, is almost universally prescribed to patients who have had an MI.24 When aspirin is given, platelets' thromboxane B2 (TXB2)-generation is impaired.25 The existence of impairment in TXB2-generation could therefore be used as a measure of aspirin's effect.18 Although a biological resistance to aspirin may also account for lack of effect, in clinical practice, a lack of aspirin effect, in the majority of cases, is indicative of non-adherence.20,26 In a preliminary study in 20 patients who were taking aspirin under observation, we determined the range of aspirin's effect on platelets in a group of patients whose adherence pattern was known. The ranges obtained in this preliminary cohort were used to determine the aspirin effect status in patients in the main cohort (effect: Yes/No). Serum TXB2 levels were assayed with an ELISA kit (TXB2 ELISA Kit, R&D Systems, United States).

Procedure
The Impact of Event Scale (IES)22,27 was obtained at screening for all patients. We worded the questionnaire to reference the MI as the traumatic event in all questions, so as to capture, specifically, MI-related PTSD symptoms (not PTSD related to other events in the patient's history). We did that because non-adherence to medical recommendations is likely related specifically to MI-related PTSD (through avoidance of reminders of the MI). Patients who had threshold scores (≥17 on both subscales)18 on the IES were asked to take a more extensive PTSD scale (the Posttraumatic Diagnostic Scale [PDS]),28 were given an educational session explaining the importance of adherence to medical recommendations post-MI, and were offered clinical assessment and a manual-based, trauma-focused course of CBT. Patients who agreed to psychiatric assessment and treatment participated in a baseline clinician-administered diagnostic psychiatric interview (the Structured Clinical Interview for DSM-IV [SCID]),29 and were asked to answer a self-report depression questionnaire (the Beck Depression Inventory [BDI]),30 as well as the PTSD questionnaires (the IES, PDS) pretreatment and at follow-up. The reason we included a depression questionnaire in the assessment of patients who received treatment for PTSD is that PTSD is frequently comorbid with depression, and treatment of PTSD31 has been shown (in other settings) to improve depressive symptoms, as well.32–34 We wished to explore whether trauma-specific treatment seems to improve depression, as well as PTSD, post-MI.

Table 1 summarizes the measures that were used for each group of patients.


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TABLE 1. Timing of Assessments



Psychiatric Measures
The Impact of Event Scale (IES)22,27 is a 15-item, self-report questionnaire composed of two scales, the 7-item Intrusion subscale and the 8-item Avoidance subscale. The authors of the scale have suggested that, for the subscales, low scores are those<8, medium scores are 8–16, and high scores are ≥17. IES scores have shown good-to-high internal consistency. Cronbach alpha ranged from 0.79 to 0.92 for the Intrusion subscale and from 0.73 to 0.91 for the Avoidance subscale. Test–retest reliability for the total score (N=20) was r=0.93 over a 1-week interval.35 The IES has been extensively used in clinical and nonclinical populations.35 The IES has the advantage of being brief, and it has been a predictor of non-adherence in the previous reports.12,18 The cutoff that we used is a score ≥17 on both the Avoidance and the Intrusion scales.

The Beck Depression Inventory (BDI)30 is a 21-item, self-report measure of depression that has been shown in previous research to have good reliability and validity. The BDI's internal consistency ranges from 0.58 to 0.93, and test–retest reliability estimates range from 0.69 to 0.90.35

The Posttraumatic Stress Disorder Diagnostic Scale (PDS)28 is a self-report measure of PTSD. As compared with the IES, the PDS is geared toward a DSM–IV diagnosis, and it assesses all symptom domains. We used this more-detailed instrument along with the IES in identified patients. Participants are asked to rate, with respect to the MI, how much they are bothered by each of the 17 PTSD symptoms specified in the DSM–IV, on a scale ranging from 0 (not at all or only one time) to 3 (5 or more times per week/almost always). Also, they indicate whether or not the symptoms interfere with a variety of areas of their lives. The PDS yields a measure of PTSD severity that we used to gauge apparent treatment effects. It demonstrated high internal consistency (r=0.92) and good test–retest reliability for the diagnosis of PTSD (r=0.74) and symptom severity (r=0.83). It showed good diagnostic agreement with the SCID and good sensitivity and specificity (r=0.65; agreement: 82%; sensitivity: 0.89; specificity: 0.75).

The Structured Clinical Interview for DSM–IV (SCID)29 was used to assess Axis I diagnoses. The SCID has acceptable interrater reliability and test–retest reliability ({kappa}s between 0.70 and 0.94).

Treatment
All of the patients who met the IES threshold criterion were given one educational session in which the importance of adherence to medications was stressed. Furthermore, all of these patients were contacted by telephone bi-weekly, two or three times, to encourage adherence to medical recommendations. For clinical reasons, this was considered to be the minimal ethically required intervention, because of the known association between PTSD and non-adherence.18 All of these patients were told that the treatment of PTSD post-MI has not been proven to be effective, and they were then offered the option of continuing with a more thorough psychiatric assessment and treatment if they wished to receive it. The PTSD treatment consisted of four or five CBT sessions. This was an abbreviated relaxation/exposure/cognitive-reprocessing approach, which incorporated the principles of PTSD treatment as developed by Foa et al. (described in detail elsewhere).31 Treatment followed a written manual and was administered by a psychiatrist.

Patient Groups
We expected to include the following groups of patients:

  1. Patients who did not meet the PTSD threshold criterion, and were not given any treatment: These patients were followed in order to observe the natural progression of cardiovascular risk profile and PTSD symptoms in these MI survivors without initial PTSD.
  2. Patients who met the IES threshold PTSD criterion in screening but either did not want to receive psychiatric treatment, or agreed but did not come to subsequent sessions: These patients received the initial educational session and several (two or three) telephone reminders and were then followed.
  3. Patients who met the IES threshold PTSD criterion in screening, chose to receive treatment, and came to the CBT sessions: These patients were treated by a psychiatrist and were followed.

Statistical Analyses
Thromboxane-generation cutoff: The preliminary TXB2-generation tests yielded a range of TXB2-generation values for patients who were taking aspirin under observation. We arbitrarily decided to determine the cutoff point for "no aspirin effect" (corresponding to non-adherence) as five standard deviations (SDs) above the mean value obtained for patients who were taking aspirin. Choosing this five-SD margin ensures a high level of confidence (p<0.0001) that patients who fall above the threshold indeed do not have a full effect of aspirin, which is the reason for choosing this restrictive cutoff. Nevertheless, because this cutoff point is arbitrary, we also present analyses that used the TXB2-generation test as a continuous, rather than a dichotomous, variable.

Other Analyses
Follow-up observations were analyzed by use of a Completer analytic model for the differences in medical and psychiatric outcomes and adherence variables. We chose to use a Completer analysis, rather than an intent-to-treat model, because the treatment phase was not randomized, and, in a nonrandomized allocation, intent-to-treat analysis accentuates the effect of patients' choices of whether or not to receive treatment on the final results; p values of ≤0.05, two-tailed, were regarded as significant. Treatment comparisons were made with Fisher's exact test and Student's t-test. Because of the small sample size and the fact that TXB2 values were not normally distributed, we did not use multivariate analytic methods.


  RESULTS

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
DISCUSSION
 CONCLUSION
 REFERENCES
 
Preliminary TXB2 Determinations
Following a method that we described in detail elsewhere,20 blood samples from 20 patients taking aspirin 100 mg/day under direct observation were used in order to determine "cutoff" values for aspirin effect. TXB2 levels are expressed in ng/ml. The range of TXB2-production was 1.1–5.7, and the mean (SD), in ng/ml, was 3.3 (1.75). On the basis of these results, the cutoff value determined for no aspirin effect (non-adherence) was 12 ng/ml.

Main Cohort
Of the 100 patients who were approached during the study period, 65 consented and were screened. Of these, 14 (22%) met the PTSD questionnaire screening threshold criterion and were offered a full psychiatric evaluation and treatment. Baseline values are presented in Table 2.


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TABLE 2. The Risk-Factor Profile in Patients Examined at Baseline (6–9 Months After an Acute Myocardial Infarction [MI])



Baseline Differences Between Patients Who Scored Above and Below the Predetermined PTSD Symptom Score
At baseline (6–9 months after an acute MI), patients reporting threshold PTSD symptoms had more cardiovascular risk factors than patients without PTSD (2.2 [1.1] versus 1.1 [1.1]; p=0.0025; Table 2). When comparing each individual risk factor, most risk factors were less controlled in patients with PTSD than in those without (Table 2), and some of these differences reached statistical significance.

Follow-Up at 6 Months (in Treated and Non-Treated Patients)
Seven of the 14 patients with threshold PTSD scores agreed to psychiatric evaluation and treatment; 6 of the 7 came to at least 3 sessions. One patient did not come to any CBT session and was therefore included in the "no-CBT" group, for a total of 6 patients who actually received CBT and 8 patients who actually did not receive CBT (these groups were used in the completer analyses). All patients agreed to be followed. There were no significant baseline differences in the values of the parameters listed in Table 2 between patients who decided to receive psychiatric treatment and those who decided not to.

Psychiatric Evaluation
SCID interviews were conducted with the seven patients who agreed to further evaluation and treatment and with two others who did not agree to treatment but wanted the evaluation. These interviews revealed that six patients had PTSD (one with comorbid major depressive disorder); two did not meet DSM-IV criteria for PTSD, but had an adjustment disorder; and one had a major depressive disorder with psychotic features. Six patients with PTSD and one patient with adjustment disorder agreed to treatment. Despite agreeing to treatment, the patient with adjustment disorder eventually did not come to the CBT sessions.

Changes in Psychiatric Symptoms
Table 3 summarizes the change in psychiatric symptom scores between the groups. Patients without PTSD (by symptom-cutoff determinations) and patients with PTSD who were not treated had only a very small and insignificant change in their PTSD symptom scores between the baseline and follow-up assessments (on average, +0.5 points in patients without PTSD, –1.6 points in those with threshold PTSD symptoms who were not treated). In contrast, patients with threshold PTSD scores who agreed to be treated reported a significant improvement in PTSD symptoms (on both the PDS and IES scales) at the end of the study. Patients who agreed to treatment also reported an improvement in their depression symptoms (BDI scores), but this improvement did not reach statistical significance.


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TABLE 3. Psychiatric Symptom Scores at Baseline and Follow-Up in the Various Patient Groups



Change in Medical Risk-Factor Score and in Individual Risk Factors During Follow-Up
Table 4 summarizes the change in medical variables in patients who received versus those who did not receive CBT intervention. In summary, patients with threshold PTSD scores who received specific PTSD treatment (as compared with a nonspecific behavioral/educational intervention) had an improvement in most medical risk factors at 6 months, when compared with their baseline (significant improvements were noted in blood pressure control, smoking, cholesterol levels, and aspirin adherence in patients who received the CBT module, whereas patients who received only the nonspecific intervention improved only in aspirin adherence). Patients with low PTSD scores ("No PTSD") had no change in their medical risk.


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TABLE 4. Medical Variables at Baseline and Follow-Up in the Various Patient Groups



Adherence to Aspirin Treatment
TXB2-generation was significantly less impaired (less aspirin effect) at baseline in patients who had threshold levels of PTSD symptoms when compared with those who did not have symptoms. This was true whether TXB2-generation was examined as a dichotomous or as a continuous variable (Table 2). We observed substantial improvement in TXB2-generation in patients with PTSD who were given either the nonspecific educational/behavioral approach (which targeted non-adherence) or the psychiatric treatment-plus-education (Table 4).


  DISCUSSION

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
CONCLUSION
 REFERENCES
 
In this cohort, symptoms of posttraumatic stress are associated with poor cardiovascular risk-factor control in patients with cardiovascular illness. Patients who were traumatized by the MI were also more likely to be non-adherent to prescribed aspirin. Examining previous cohorts, we reported that substantial PTSD symptoms post-MI are associated with non-adherence to captopril12 and aspirin18 and with an increased likelihood of cardiovascular readmissions post-MI.18 We believe that a likely explanation for the association between posttraumatic stress and poor cardiovascular risk-factor control post-MI is that PTSD leads to non-adherence to medical recommendations. However, our cross-sectional data cannot substantiate a cause-and-effect relationship.

The preliminary results we present here show that cognitive-behavioral (CBT) treatment of PTSD could potentially help improve psychiatric symptoms (PTSD as well as depression) and medical risk-factor control in affected patients. Moreover, a nonspecific educational/behavioral intervention seemed to be helpful in improving adherence to the aspirin regimen in PTSD patients, even in the absence of a specific PTSD treatment module. Nonspecific interventions that focus on adherence are easier to administer, do not require a mental health professional, and could therefore be the first line of treatment in affected patients who either will not or cannot participate in a CBT course. Although these results are certainly encouraging, only a randomized, controlled treatment study could establish whether any treatment indeed improves outcome.

Previous studies have investigated the relative contribution of PTSD to medical morbidity, as compared with comorbid depressive and general distress/anxiety symptoms, in patients with cardiovascular illnesses.12,18,19 All of these studies found that PTSD symptoms are stronger predictors of poor outcome than are symptoms of depression or general distress. In our study, consistent with reports in the PTSD treatment literature,33,34 symptoms of depression seemed to improve as well as PTSD symptoms after treatment. However, this improvement was not statistically significant.

Our specific measure of adherence to medications was platelets' thromboxane B2-generation (a measure of aspirin intake). Certainly, a lack of aspirin effect can also be due to a biological resistance to aspirin (aspirin-resistance). Because we observed changes in aspirin response even after one educational session (in the PTSD non-treated patients), it is likely that aspirin non-response was primarily related to non-adherence in our study. A biological resistance to aspirin is not expected to disappear after education about the importance of taking aspirin. This result is consistent with published results20,26 that aspirin non-response post-MI is mainly due to non-adherence, rather than a biological resistance.

We believe that the association that we observed between PTSD symptoms and poor cardiovascular risk-factor control post-MI is mainly due to non-adherence to medical recommendations in patients who are emotionally traumatized by the MI. However, PTSD symptoms may also affect cardiovascular outcome via biological pathways that are directly related to PTSD: PTSD is associated with increased heart rate and with altered reactivity of the hippothalamo-pituitary-adrenal axis,36 both of which may affect the cardiovascular system. Future studies could try to address the reasons for the association that we observed—is it only because of impaired adherence in patients with PTSD, or also because of the biological correlates of posttraumatic symptoms. Furthermore, it is plausible that medical events, such as a previous MI (occurring before the index MI which was used as enrollment criterion for our study), as well as previous traumatic events of any kind, may have made patients more susceptible to the development of posttraumatic symptoms following the index event.37 The present study did not address the reasons for susceptibility to develop PTSD post-MI. In the future, factors that determine vulnerability (or resilience) to post-MI traumatic stress could be identified and may be used to inform treatment options.

Study Limitations
The present study should be viewed as an exploration into a newly recognized, and possibly treatable, risk factor for non-adherence and poor risk-factor control post-MI. It is limited by the relatively small sample size and by the fact that only 65 of the 100 eligible patients agreed to participate. The study was not designed to evaluate the effects of treatment and should not be interpreted as proof of treatment efficacy. A controlled, randomized study is needed before firm conclusions can be made regarding treatment efficacy. Furthermore, it should be noted that our threshold symptom criterion for PTSD was based on the IES score. The score is associated with, but is not the same as, the existence of the psychiatric diagnosis of PTSD in the assessed patients.


  CONCLUSION

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 CONCLUSION
REFERENCES
 
A myocardial infarction can be emotionally traumatic. PTSD is a specific anxiety disorder that follows exposure to a traumatic experience. The present study and previous ones point to PTSD as a relatively common and potentially important cause of medication non-adherence and, hence, poor risk-factor control in MI survivors. Clinicians who treat patients who have had an MI should be aware of PTSD symptoms in these patients. If the results of the present study are replicated in further research, addressing patients with PTSD either in a nonspecific intervention to improve adherence or, preferably, using specific techniques for the treatment of PTSD, could become a new strategy to improve psychiatric outcomes and medical risk-factor control post-MI. Randomized, controlled treatment studies should be conducted before any firm treatment recommendations can be made.


  ACKNOWLEDGMENTS

 
The authors thank Edna B. Foa, Ph.D., for her important contribution to the development of the ideas that are presented in this article.

The work represented in this article was partially supported by NIH grants MH 63755 and MH 071249 to Eyal Shemesh, M.D., and by a grant from the Y.H. Mirzoeff and Sons Foundation, Inc.


  REFERENCES

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 

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