(Circulation. 1996;93:1170-1176.)
© 1996 American Heart Association, Inc.
Articles |
Sex Differences in Cardiac Arrest Survivors
From Massachusetts General Hospital, Boston.
Correspondence to Christine Albert, MD, Cardiac Unit, Bulfinch 2, Massachusetts General Hospital, 32 Fruit St, Boston, MA 02114.
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Abstract |
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Background Important sex differences in the epidemiology of sudden death and in the results of electrophysiological testing in survivors of cardiac arrest have been identified. These differences are currently poorly understood.
Methods and Results Three hundred fifty-five consecutive survivors of out-of-hospital cardiac arrest (84 women and 271 men) referred for electrophysiologically guided therapy were analyzed retrospectively for sex differences in underlying pathology and predictors of outcome. Women were significantly less likely to have underlying coronary artery disease than men (45% versus 80%) and more likely to have other forms of heart disease or structurally normal hearts (P<.0001). The mean left ventricular ejection fraction was higher in women (0.46±0.18 versus 0.41±0.18, P<.05), and women were more likely to have no inducible arrhythmia at baseline electrophysiological testing (46% versus 27%, P=.002), although when the patients were stratified by coronary artery disease status, these sex differences were no longer present. The independent predictors of outcome differed between men and women. In men, a left ventricular ejection fraction of <0.40 was the most powerful independent predictor of total (relative risk, 2.8; 95% CI, 1.6 to 5.0; P<.0001) and cardiac (relative risk, 6.3; 95% CI, 2.9 to 13.5; P<.0001) mortality. In contrast, the presence of coronary artery disease was the only independent predictor of total (relative risk, 4.5; 95% CI, 1.5 to 13.4; P=.003) and cardiac (relative risk, 4.4; 95% CI, 1.2 to 15.6; P=.012) mortality in women.
Conclusions Female survivors of cardiac arrest are less likely to have underlying coronary artery disease. The predictors of total and cardiac mortality differ between male and female survivors. Coronary artery disease status is the most important predictor in women, and impaired left ventricular function is the most important predictor in men.
Key Words: death, sudden • women • arrhythmia • electrophysiology • fibrillation
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Epidemiological studies1 2 3 4 and outcome data from clinical trials of acute myocardial infarction5 6 have identified sex differences in the incidence and risk factors for sudden death. Women are at decreased risk at all ages, constituting only 21% of ventricular fibrillation arrest victims in Seattle4 and 32% of sudden death victims in the Framingham study.1 Nevertheless, sudden death is still an important cause of cardiovascular mortality in women. In women, 64% of sudden deaths compared with 50% in men occur in persons without prior clinical evidence of coronary heart disease, and therefore, sudden death is often the first manifestation of heart disease.2 Efforts to prevent sudden death have been directed at the prevention of coronary artery disease, but the classic coronary risk factors do not appear to predict sudden death to the same degree in women as they do in men.1 2
There have also been reports of sex differences in the results of electrophysiological testing in survivors of cardiac arrest. Women have been reported to be less likely to have inducible ventricular arrhythmias during programmed ventricular stimulation.7 8 9 The causes of these sex differences in sudden death victims and cardiac arrest survivors are poorly understood. In an attempt to further understand these differences, we analyzed retrospectively a large referral population of 355 consecutive cardiac arrest survivors for sex differences in their underlying cardiac pathology, electrophysiological characteristics, and predictors of outcome.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patient Population
The study was a retrospective analysis of 355 consecutive survivors of out-of-hospital cardiac arrest who were referred to the Cardiac Arrhythmia Service of the Massachusetts General Hospital for electrophysiologically guided therapy from January 1978 to December 1992. External electrical defibrillation was required for resuscitation in all cases. Patients were excluded if the cardiac arrest occurred during hospitalization or if subsequent evaluation revealed evidence of a new Q-wave myocardial infarction. There were 84 women and 271 men in the study population. The mean age (±SD) of the patient population was 57.3±13.7 years. Two hundred fifty-four patients (71.5%) had coronary artery disease (defined as
70% stenosis in one or more epicardial arteries
and/or evidence of old myocardial infarction or ischemia) as
their principal cardiac abnormality. The mean left
ventricular ejection fraction (LVEF) was 41.8±18.6%, and
170 patients (47.9%) had an LVEF of <40%. The rhythm documented at
cardiac arrest was ventricular fibrillation in 321 patients
(90.4%), ventricular tachycardia in 30
patients (8.5%), and unknown in 4 patients.
Management
Baseline Evaluation
After the
patients had recovered from the presenting cardiac
arrest, cardiac catheterization with coronary
arteriography and left ventriculography was performed in all except 11
patients (3.1%). All patients underwent noninvasive assessment of left
ventricular function. Three hundred thirty-three
patients (94%) underwent baseline
electrophysiological testing in the absence
of antiarrhythmic drugs unless clinical instability made antiarrhythmic
drug withdrawal impossible. In 22 patients (8.8%) with critical
coronary artery stenoses and/or unstable
ischemic symptoms,
electrophysiological testing was deferred
until after coronary revascularization.
Initial electrophysiological testing was
performed a mean of 3.9±6.0 days after resuscitation.
Electrophysiological studies were performed with a programmable stimulator with a constant current source delivering 2-ms rectangular pulses at fivefold diastolic threshold. The protocol for ventricular stimulation included introduction of single and double extrastimuli after pacing drive trains at a minimum of two basic cycle lengths (600 and 400 ms) and at two right ventricular sites in all patients. In studies before 1982, brief bursts of rapid ventricular pacing (5 to 10 beats at cycle lengths of 400 to 220 ms) were used. In 1982 and subsequent years, the protocol included triple ventricular extrastimuli instead of burst pacing. The end point of the stimulation protocol was the induction of sustained ventricular arrhythmia lasting more than 30 seconds or causing hemodynamic deterioration requiring intervention. Before 1982, the reproducible induction of nonsustained ventricular tachycardia (5 to 100 beats) was also used as an end point.
Treatment
Coronary
artery revascularization,
with coronary artery bypass surgery (107 patients) or
percutaneous coronary angioplasty (5 patients),
was performed in 112 patients (31.5%) with evidence of significant
coronary artery stenoses and reversible myocardial
ischemia. Map-guided left ventricular
aneurysmectomy was performed in 4 patients, and valve
replacements were performed in another 4 patients.
Patients with inducible sustained ventricular arrhythmias underwent serial drug testing to identify an antiarrhythmic regimen that suppressed the induced ventricular arrhythmia. A favorable drug response was defined as the induction of fewer than 10 repetitive ventricular complexes in response to completion of the programmed stimulation protocol. Before the availability of the implantable cardioverter/defibrillator (ICD), patients were discharged on the drug regimen shown to prevent initiation of the ventricular arrhythmias induced at baseline electrophysiological study. If no drug suppressed the arrhythmia, drugs that rendered the arrhythmia more difficult to induce, slower in rate, or better tolerated were used. From 1983 on, placement of an ICD was recommended in patients who had persistently inducible sustained ventricular arrhythmias despite pharmacological and/or surgical therapy. Placement of an ICD was also recommended for patients who had no inducible sustained ventricular arrhythmia at baseline electrophysiological study and who did not have critical coronary artery disease requiring revascularization or another reversible cause for cardiac arrest.
Patient Follow-up
Personal or
telephone contact was made with all patients or
their physicians or family members, and the circumstances of any deaths
were investigated to determine probable cause. Sudden cardiac death was
defined as death that occurred as a result of recurrent cardiac arrest
(sudden unexpected circulatory collapse) or within 1 hour of the
development of symptoms in a previously stable patient or an
unwitnessed death in a patient known to be stable in the preceding 24
hours. Nonsudden cardiac death was defined as death due to progressive
heart failure or recurrent myocardial infarction and/or with preceding
symptoms of more than 1 hour in duration.
Statistical Analysis
Baseline patient characteristics are
expressed as mean±SD for
continuous data and proportions for categorical data. Comparisons
between men and women were made by unpaired t tests,
2 analysis, or Fisher's exact test as
appropriate.
The effect of relevant covariates (predictors) on total
mortality,
cardiac mortality, and sudden death were evaluated in the entire
population and in men and women separately by stepwise
multivariate regression analysis using a Cox
proportional-hazards model.10 Fifteen covariates
(listed in Table 4
) were entered into the model. After initial
screening of the univariate significance of the individual
variables in the Cox model, relationships for which the probability
value approached significance (P<.10) were investigated
further within the framework of stepwise multiple Cox regression to
examine their joint and relative effects on outcome (BMDP Statistical
Software: P2L).11 The relative risk and 95% confidence
interval for the regression parameter associated with each
variable that reached significance (P<.05) in the final
model were calculated. Kaplan-Meier survival curves for men and women
were calculated with the program BMDP:P1L.12
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Baseline Characteristics
Clinical Characteristics
There were 271 men and 84 women in the database. The clinical and electrophysiological characteristics of the men and women are presented in Table 1
. Several
clinical features differed between the men and the women. Women were
significantly less likely to have coronary disease as their
underlying cardiac abnormality. There were 216 men (80%) with
coronary artery disease compared with only 38 women (45%).
Women were also less likely to have suffered a prior myocardial
infarction (33% versus 47%). The mean LVEF was higher in the women at
0.46±0.18 compared with 0.41±0.18 in the men. The sexes did not
differ with respect to age, past history of congestive heart failure,
left ventricular aneurysm, antiarrhythmic drugs at
cardiac arrest, or treatment with ß-adrenergic
antagonists.
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Underlying Structural Heart Disease
Fig 1 illustrates the proportion of various types
of structural heart disease in the male and female cardiac arrest
survivors. A large majority (80%) of the men had coronary
artery disease as their principal diagnosis. The remaining 20% had
primarily dilated cardiomyopathy (10%) and
valvular heart disease (5%). In contrast, 55% of the women
had nonischemic heart disease, including dilated
cardiomyopathy (19%), valvular heart
disease (13%), and coronary vasospasm (5%), which was
uncommon in the men. Ten percent of women as opposed to 3% of men had
structurally normal hearts. This difference in the distribution of
underlying structural heart disease was significant when
analyzed by 2 analysis
(P<.0001).
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Electrophysiological Testing and
Treatment Regimens
The results of baseline
electrophysiological testing (Table 1
)
differed significantly between men and women. Forty-six percent of
the women versus 27% of the men had no inducible arrhythmia at
baseline testing (P=.002). The greatest difference occurred
in the subgroup with inducible sustained monomorphic
ventricular tachycardia. Twenty-four
percent of women versus 36% of men had this end point during
programmed ventricular stimulation (P<.05). Men
and women did not differ significantly in the distribution of results
at predischarge electrophysiological
testing and in the likelihood of antiarrhythmic drugs and/or surgery
suppressing inducible ventricular arrhythmias.
Similar proportions of men and women were discharged on antiarrhythmic
drugs or ß-adrenergic antagonists (Table 2). Women were
significantly less likely to undergo
coronary artery bypass graft surgery (P<.05) during
the hospitalization, and a higher percentage of women underwent ICD
therapy, although this difference was not statistically
significant.
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Results Stratified by Coronary Artery
Disease
Given the large sex difference in the proportion of patients
with
coronary artery disease, we stratified the population according
to the presence or absence of underlying ischemic heart disease
and again compared the men and the women in each subgroup (Table
3). The men and women in the subgroup with
coronary artery disease did not differ with respect to age,
number of critically stenosed vessels at angiography, history of prior
myocardial infarction, LVEF, or results of
electrophysiological testing. The same
proportion of women and men with coronary artery disease
underwent coronary artery bypass surgery. In the subgroup
without ischemic heart disease, women were still more likely to
have no inducible arrhythmia at baseline
electrophysiological testing, although this
was only of borderline significance. There were no significant sex
differences with respect to age and LVEF. The subgroup of patients
without ischemic heart disease had a higher mean LVEF
(0.49±0.19) and a lower mean age (48±17 years) than the patients
with
ischemic heart disease. Thus, the sex differences observed in
LVEF and responses to electrophysiological
testing in the entire population are due primarily to the sex
difference in the prevalence of coronary artery disease.
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Survival
Eighty-six deaths occurred over a median follow-up
of 24.4
months: 19 deaths in women and 67 in men. The cumulative survival for
the entire group at 5 years was 70% and at 10 years, 44%. The median
follow-up did not differ significantly between men and women (23.5
months in men and 29.7 months in women). When analyzed by
life-table survival analysis, men and women did not differ
with respect to their overall survival, as seen in Fig 2.
Similarly, there was no sex difference in survival
free of cardiac mortality or sudden death.
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Predictors of Mortality
Total Population
All
variables analyzed as predictors of total,
cardiac, and sudden death mortality are listed in Table 4. The
univariate significance for cardiac
mortality for each of these predictors is also shown. The independent
predictors from the multivariate Cox regression model
and the relative risks and 95% confidence limits for the entire
population are displayed in Table 5. LVEF <0.40 was the
most important independent predictor of total mortality, with a
relative risk of 2.9 (95% CI, 1.8 to 4.6). Other independent
predictors of total mortality included age (relative risk, 1.5 per
decade of life; 95% CI, 1.2 to 1.8) and sustained monomorphic
ventricular tachycardia at predischarge
programmed ventricular stimulation (relative risk, 2.2;
95% CI, 1.4 to 3.7). ICD therapy was a negative predictor, with a
relative risk of 0.5 (95% CI, 0.3 to 0.8).
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LVEF <0.40 was again the most powerful predictor of cardiac mortality (relative risk, 4.6; 95% CI, 2.5 to 8.7). The presence of coronary artery disease and absence of an ICD were also independent predictors of cardiac mortality. The presence of an ICD was a powerful negative predictor of sudden death (relative risk, 0.18; 95% CI, 0.05 to 0.61), and sustained monomorphic ventricular tachycardia at predischarge programmed ventricular stimulation was a positive predictor of sudden death (relative risk, 3.6; 95% CI, 1.5 to 3.6). Of note, sex did not predict total, cardiac, or sudden death mortality in the univariate or multivariate analysis.
Sex-Specific Predictors of Outcome
Given
the differences between men and women in their clinical and
electrophysiological characteristics and
underlying structural heart disease, we postulated that there may also
be different predictors of outcome in women versus men. Table 6
lists the results of the multivariate
Cox model when the men and women were analyzed separately. The
predictors of mortality in men for the most part resembled those in the
total population. An LVEF of <0.40 was the most powerful independent
predictor of cardiac and total mortality, with relative risks of 6.3
(95% CI, 2.9 to 13.5) and 2.8 (95% CI, 1.6 to 5.0), respectively. ICD
therapy was the most important negative predictor of sudden death, with
a relative risk of 0.05 (95% CI, 0.01 to 0.39). Coronary
artery disease was not an independent predictor of cardiac
mortality in the men, as it was in the total population.
Discharge on antiarrhythmic drugs replaced ICD therapy and
sustained monomorphic ventricular tachycardia
at predischarge electrophysiological study
as an independent predictor of total mortality in men. It is notable
that antiarrhythmic drugs were associated with worsened overall
survival, whereas ICD therapy was associated with improved survival
from cardiac mortality and sudden death.
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The results for women differed from those for the entire population and from those observed in men. In women, the presence of coronary artery disease was the only independent predictor in the multivariate Cox model of cardiac and total mortality, with relative risk of 4.4 (95% CI, 1.2 to 15.6) and 4.5 (95% CI, 1.5 to 13.4), respectively. Fifteen of the 19 deaths in women (79%) were in the subgroup with coronary artery disease. The smaller sample size of women is reflected in the wide CIs, and other predictors might have reached significance in a larger sample. This may explain, in part, why LVEF and ICD therapy were not found to be predictors in women as they were in men. The only predictor of sudden death in women was the presence of a left ventricular aneurysm, a marker for both a large myocardial infarction and coronary artery disease. Six of eight of the sudden deaths occurred in the patients with coronary artery disease. ICD therapy was not a predictor of sudden death in women, although the small number of sudden deaths in women limits the ability to accurately determine predictors of this outcome.
Surprisingly, LVEF was not even a univariate predictor
of
total mortality in women. It was a univariate predictor of
cardiac mortality, but it was not as powerful as coronary
artery disease and was not an independent predictor in the
multivariate analysis. This finding did not
change if LVEF was analyzed as a continuous variable or as
a dichotomous variable with a cutoff at 0.30 versus 0.40. The
independent effects of coronary artery disease and LVEF on
survival in women are demonstrated in Fig 4. Women were
stratified by LVEF <0.40 or 0.40 and the presence or absence of
coronary artery disease, and actuarial survival
analysis was performed on the four groups. The two groups of
women with coronary artery disease had a similar survival at 5
years (63% for those with an LVEF <0.40 versus 65% for those with an
LVEF 0.40), which was worse than the 5-year survival in the two
groups without coronary artery disease (100% for the low-LVEF
group and 85% for the high-LVEF group).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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In this referral population of 355 consecutive survivors of out-of-hospital cardiac arrest, sex differences exist in the underlying cardiac pathology and predictors of outcome. Most notably, women are a much more heterogeneous population than men. The distribution of underlying structural heart disease is not consistent with our current concept of cardiac arrest survivors.12 Female survivors of cardiac arrest are less likely to have underlying coronary artery disease and more likely to have other forms of heart disease or structurally normal hearts. This may explain, in part, why the classic risk factors for coronary artery disease do not predict sudden death as well in women in the Framingham Heart Study. Only hypertension and smoking conferred a long-term risk of sudden death in women, and to a lesser extent than in the men.1 Diabetes and hypercholesterolemia, which are strong risk factors for coronary artery disease in this population of women,13 were not associated with sudden death.1 Possible explanations for the lower incidence of sudden death in women and the lower frequency of coronary artery disease in female cardiac arrest survivors may be the lower incidence of coronary artery disease in women before age 65 years14 and/or an intrinsic protective effect against sudden death associated with being female in patients with coronary artery disease. The proportion of coronary heart disease deaths that were sudden was also lower in women (34% versus 46% in men) in the Framingham Study.1
The women in our population as a whole had higher LVEFs and were less likely to have inducible ventricular arrhythmias during programmed ventricular stimulation. This is not surprising, given the lower frequency of coronary artery disease and the larger percentage of structurally normal hearts in the women. The differences in LVEF and electrophysiological study results between men and women were no longer present once the patients were stratified by coronary artery disease status, except for the responses to electrophysiological testing in the subgroup without coronary artery disease. In this subgroup, women were less likely to have inducible sustained ventricular arrhythmias at baseline testing. This difference was of borderline statistical significance and may again be due to the higher percentage of structurally normal hearts in the women. These findings are in contrast to a smaller study8 of 13 women with coronary artery disease that found that women in this subgroup were less likely than men to have inducible ventricular arrhythmias. In our population, the results of electrophysiological testing in women with coronary artery disease were nearly identical to those observed in men.
Although total, cardiac, and sudden death mortality did not differ
between men and women, the independent predictors of outcome were
different. The predictors in men resembled those of the total
population, which was expected, given the male predominance of the
study population. One exception, however, was the presence of
coronary artery disease, which was a significant predictor of
cardiac mortality (P=.007) in the total population but was
not a predictor in men. In contrast, the only independent predictor of
cardiac mortality and total mortality in women was the presence of
coronary artery disease. The women with coronary artery
disease were 4.5 times more likely to die and 4.3 times more likely to
die of a cardiac cause than women without coronary artery
disease. Therefore, while coronary artery disease was less
common in female cardiac arrest survivors, those survivors with
coronary artery disease had a worse prognosis. Although the
explanation for this finding is unknown, it is possible that women with
coronary artery disease who present with a cardiac arrest
may have a more aggressive form of the disease, which is associated
with a poor prognosis. Conversely, the women without coronary
artery disease had a surprisingly good prognosis (Fig 4) even
in the
presence of impaired left ventricular function.
LVEF, which was the strongest independent predictor of total and cardiac mortality in men, did not have the same significance in the women. LVEF was not a significant univariate predictor of total mortality and was not an independent predictor of cardiac mortality in women once coronary artery disease status was accounted for. It is unclear why LVEF did not predict mortality to the same degree in female cardiac arrest survivors. Two studies5 15 have brought into question the importance of LVEF in prognosis after myocardial infarction in women. In the MILIS study, women were found to have a worse prognosis after myocardial infarction despite having had higher LVEFs at hospital discharge, suggesting that the prognostic information derived from this variable may differ between men and women.15 In a considerably larger population of post–myocardial infarction patients that included 538 women, Dittrich et al5 also found that the women had higher LVEFs. That study examined prognostic variables in men and women separately and found that female survivors and nonsurvivors were equally likely to have an LVEF of <0.40. The male nonsurvivors, however, were significantly more likely to have an LVEF of <0.40 than the survivors. Another study6 that examined this issue found that an LVEF of <0.40 after myocardial infarction was predictive of mortality in women and men but that frequent ventricular premature beats, which were a predictor in men, were not predictive of outcome in women.
Finally, ICD therapy, which was a negative predictor of cardiac mortality and a very powerful negative predictor of sudden death in men, was not a predictor of either end point in women. This may be due, in part, to the smaller number of each of these end points in the women (only 8 sudden deaths) and therefore insufficient power to detect ICD therapy as a predictor rather than a true sex difference. However, if the strength of the association in men (relative risk of 0.05) had also been present in women, it probably would have been detected.
Study Limitations
The primary limitations of this study are
its retrospective
design, referral-based population, and smaller number of women in
the study. Despite the nonrandom allocation of treatment, it is
unlikely that significant bias occurred in the treatment of men versus
women, since they did not differ significantly with respect to the
major treatment modalities (Table 2), with the exception of
coronary artery bypass surgery, which was explained by the
lower prevalence of coronary artery disease in women (Table 3).
This referral-based population may not be
representative of the general population of sudden
death victims or cardiac arrest survivors owing to referral bias. It is
unlikely that women were selectively not referred for
electrophysiological testing, given the
similar percentage of women in this study (23.6%) compared with a
population-based cohort in Seattle (21%).4 The mean
age of this population was slightly lower at 57.3±13.7 versus
63.8±12.2 years in the survivors of out-of-hospital
ventricular fibrillation arrest in Seattle. There may be
referral bias against older patients, which may decrease the amount of
coronary artery disease in the referral population, especially
in women, and may have influenced our results. Finally, the small
number of women (84) compared with men (271) limits our ability to
detect all the independent predictors of outcome in women. However, the
number is sufficiently large to provide information about the relative
importance of the major predictors of outcome in women.
Study Implications
Significant differences exist in the
underlying cardiac pathology
of male and female cardiac arrest survivors. Women are less likely to
have coronary artery disease; therefore, efforts directed at
preventing coronary artery disease may not have the same impact
on the rate of sudden death in women as in men. Further understanding
of the mechanisms involved in cardiac arrests in women with
nonischemic heart disease and with structurally normal
hearts would advance our knowledge about sudden death considerably.
Women were not routinely tested for coronary vasospasm, and
provocative tests for long-QT syndrome were not routinely
done. Given the greater proportion of women with these diagnoses,
provocative testing may be worthwhile in women who survive
a cardiac arrest. Various psychosocial factors3 may also
play a role. Despite these differences in underlying pathology, the
finding that men and women have similar total, cardiac, and sudden
death mortality rates with standard12
electrophysiologically guided treatment
regimens is reassuring.
This study contains important prognostic
information that differs from
our current understanding of cardiac arrest survivors. Female survivors
who have coronary artery disease are more likely to die and to
die of a cardiac cause independent of their LVEF. This observation
raises the possibility that more aggressive use of
revascularization and pharmacological therapy for
ischemia may be appropriate in female survivors of cardiac
arrest. Also, an LVEF 0.40 may not be as reassuring in women as it is
in men. Alternatively, the group of women without ischemic
heart disease have a better prognosis than previously thought. Finally,
this study underscores the importance of examining women separately in
studies of heart disease whenever possible as well as the risks of
generalizing findings from a predominantly male population to
women.
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Footnotes |
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Reprint requests to Jeremy N. Ruskin, MD, Cardiac Arrhythmia Service, Massachusetts General Hospital, 32 Fruit St, Boston, MA 02114.
Received June 1, 1995; revision received October 19, 1995; accepted October 23, 1995.
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C. M. Albert, C. U. Chae, K. M. Rexrode, J. E. Manson, and I. Kawachi Phobic Anxiety and Risk of Coronary Heart Disease and Sudden Cardiac Death Among Women Circulation, February 1, 2005; 111(4): 480 - 487. [Abstract] [Full Text] [PDF]
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R. Lampert, C. A. McPherson, J. F. Clancy, T. L. Caulin-Glaser, L. E. Rosenfeld, and W. P. Batsford Gender differences in ventricular arrhythmia recurrence in patients with coronary artery disease and implantable cardioverter-defibrillators J. Am. Coll. Cardiol., June 16, 2004; 43(12): 2293 - 2299. [Abstract] [Full Text] [PDF]
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S. S. Chugh, O. Senashova, A. Watts, P. T. Tran, Z. Zhou, Q. Gong, J. L. Titus, and S. J. Hayflick Postmortem molecular screening in unexplained sudden death J. Am. Coll. Cardiol., May 5, 2004; 43(9): 1625 - 1629. [Abstract] [Full Text] [PDF]
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C. M. Albert, C. U. Chae, F. Grodstein, L. M. Rose, K. M. Rexrode, J. N. Ruskin, M. J. Stampfer, and J. E. Manson Prospective Study of Sudden Cardiac Death Among Women in the United States Circulation, April 29, 2003; 107(16): 2096 - 2101. [Abstract] [Full Text] [PDF]
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B. J. Kneale, P. J. Chowienczyk, S. E. Brett, D. J. Coltart, and J. M. Ritter Gender differences in sensitivity to adrenergic agonists of forearm resistance vasculature J. Am. Coll. Cardiol., October 1, 2000; 36(4): 1233 - 1238. [Abstract] [Full Text] [PDF]
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T. M. Saleh and B. J. Connell Centrally mediated effect of 17beta -estradiol on parasympathetic tone in male rats Am J Physiol Regulatory Integrative Comp Physiol, February 1, 1999; 276(2): R474 - R481. [Abstract] [Full Text] [PDF]
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T. M. Saleh and B. J. Connell Role of 17beta -estradiol in the modulation of baroreflex sensitivity in male rats Am J Physiol Regulatory Integrative Comp Physiol, September 1, 1998; 275(3): R770 - R778. [Abstract] [Full Text] [PDF]
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