(Circulation. 1997;96:2987-2991.)
© 1997 American Heart Association, Inc.
Articles |
Prospective Prognostic Assessment of Blood Pressure Response During Exercise in Patients With Hypertrophic Cardiomyopathy
From the Department of Cardiological Sciences, St George's Hospital Medical School, London, UK.
Correspondence to W.J. McKenna, MD, Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK.
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Abstract |
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Background Previous studies revealed that an abnormal blood pressure response (ABPR) during exercise was common in young hypertrophic cardiomyopathy (HCM) patients and was associated with a family history of premature sudden cardiac death (SCD). This study was performed prospectively to assess the prognostic significance of blood pressure response during exercise in young patients with HCM.
Methods and Results Maximum symptom-limited treadmill exercise testing with continuous blood pressure monitoring was performed in 161 consecutive patients 8 to 40 years old (27±9). A normal blood pressure response, defined as an increase in the systolic pressure of at least 20 mm Hg from rest to peak exercise in the absence of a fall of >20 mm Hg from peak pressure, was seen in 101 (63%). In 60 (37%), the blood pressure response was abnormal. There was no significant difference in patients with normal blood pressure response and ABPR in terms of age, sex, follow-up, or recognized risk factors for SCD. During the follow-up period (mean, 44±20 months), SCD occurred in 12 patients: 3 (3%) in the normal blood pressure response group versus 9 (15%) in the ABPR group (P<.009). ABPR had a sensitivity of 75%, a specificity of 66%, a negative predictive value of 97%, and a positive predictive value of 15% for the prediction of SCD. There was no significant difference in the incidence of other recognized risk factors between patients with SCD and the survivors.
Conclusions A normal exercise blood pressure response identifies low-risk young patients with HCM. An ABPR identifies the high-risk cohort; the low positive predictive accuracy, however, indicates that further risk stratification is warranted.
Key Words: hypertrophy • cardiomyopathy • risk factors • death, sudden • exercise
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Introduction |
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Sudden cardiac death is a common complication of HCM, especially in adolescents and young adults, in whom it may be the first clinical manifestation of the disease in previously asymptomatic patients.1-4 Data from referral centers estimate an annual incidence of SCD of 4% to 6% in adolescence and early adulthood, decreasing to 1% to 2% in later life.4-10 A major goal in the management of patients with HCM is to accurately identify the high-risk cohort so that appropriate interventions can be applied. In adults, the finding of nonsustained VT on Holter recordings11,12 identifies the high-risk cohort with a low predictive accuracy (20% to 25%). The absence of this arrhythmia identifies the majority of low-risk patients7 with a sufficient predictive accuracy (>90%) to permit reassurance. In children, adolescents, and young adults, recurrent syncope6 and family history of premature SCD5,10 are relatively specific but fail to identify the majority of young patients who die suddenly.
Exercise-induced hypotension is a well-recognized feature of HCM. Its importance was underlined by the fact that a significant number of SCDs occur during or shortly after exercise.3,4 We have previously reported that exercise-induced hypotension occurred in one third of patients with HCM.13 It was more common in the young and was associated with a family history of SCD. The observation of an abnormal BPR during exercise in 4 of 6 patients who had experienced nonfatal sudden cardiac arrest led us to conduct this prospective study to assess the prognostic significance of BPR during exercise in young patients (<40 years old) with HCM in whom the risk of SCD is highest.
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Methods |
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Between January 1987 and February 1994, 167 consecutive HCM patients
40 years old who underwent maximum treadmill exercise
testing off cardiovascular medication at St George's
Hospital, London, were selected for this study. Six patients who had
experienced nonfatal sudden cardiac arrest before the initial exercise
test were excluded from this prospective analysis. The study
then comprised 161 patients (105 men) with a mean age of 27±9 years
(range, 8 to 40 years). Symptomatic evaluation at the time
of exercise testing revealed that 61 (38%) experienced dyspnea (NYHA
functional class II in 54 and class III in 7), 65 (40%) chest pain,
and 42 (26%) one or more syncopal episodes during the preceding 5
years. Fifty-one patients (32%) had a family history of HCM, and an
additional 52 (32%) had a family history of HCM and premature SCD (at
<35 years old) among relatives. Thirty-one (19%) had nonsustained VT,
defined as more than three consecutive ventricular beats at
a rate >120 bpm during 48 hours of ambulatory ECG recordings.
The diagnosis of HCM was based on the typical clinical, ECG, and
hemodynamic features,14,15 with
left ventricular wall thickness of 
15 mm
demonstrated on two-dimensional echocardiography
(mean left ventricular wall thickness, 21.9 mm) in the
absence of any other cardiac or systemic disease that could have caused
hypertrophy.15,16 Twenty-five
patients who did not fulfill the above echo criteria but who were
obligate or proven gene carriers were included.
Treadmill Exercise Testing
The exercise test was performed as part of the initial
prospective evaluation. Before the exercise test, all cardioactive
medications were discontinued for at least 5 half-lives. All patients
were in sinus rhythm at the time of the exercise test except one who
was in atrial fibrillation. One patient had a rate-responsive
dual-chamber pacemaker implanted for atrioventricular
conduction disease.
Maximum symptom-limited treadmill exercise testing with continuous measurement of VO2 was performed with the standard Bruce protocol in 150 patients and a modified Bruce protocol in 11 who could not sustain the more aggressive protocol. ECG monitoring was performed with the Marquette Max 1 system with automatic recordings. Twelve-lead ECGs were recorded at the end of each stage and every minute during the recovery period. Systolic BP was recorded by the same trained technician by auscultation of the Korotkov sounds at the left brachial artery with a mercury sphygmomanometer. The technique required continuous inflation and deflation of the cuff to maintain contact with the Korotkov sounds. Eleven patients in whom systolic BP recording could not be accurately obtained by auscultation underwent repeat exercise BP recording with direct intra-arterial measurements from the nondominant brachial artery. BP values were recorded at rest, at 1-minute intervals during exercise, and at 30-second intervals for 5 minutes during the recovery period. A cutoff value of 20 mm Hg was used to define two BP patterns.13,17 A normal BPR was defined as a gradual increase of at least 20 mm Hg in systolic BP during exercise, with a gradual decline during recovery. An abnormal BPR included hypotensive and flat responses. A hypotensive BPR was defined as either (1) an initial increase in systolic BP with a subsequent fall by peak exercise of >20 mm Hg compared with the peak BP value or (2) a continuous decrease in systolic BP throughout the exercise test of >20 mm Hg compared with baseline. A flat response was defined by a change in systolic BP during the whole exercise period of <20 mm Hg compared with the resting systolic BP.
Respiratory gases were collected by use of a face mask firmly applied
to prevent escape of exhaled gas. Gas analysis was performed
with established methodology with a metabolic cart (Sensor
Medics Horizon MMc, Beckman Instruments) before December 1991 and a
Marquette system (Marquette Electronics) with a mass spectrophotometric
gas analyzer thereafter. A temperature-controlled polarographic
sensor with an on-board microprocessor measured the
VO2, issuing printouts of minute
ventilation, VO2 (in mL/min), carbon
dioxide production (in mL/min), and RER at 15-second intervals.
Before the study, patients were guided in the techniques of exercise
and respiratory gas collection. Peak
VO2 was defined as
VO2 (in mL ·
min-1 ·
kg-1) at peak exercise calculated as the
mean values of the four samples taken during the last minute of
exercise. Patients were encouraged to continue the exercise test until
their RER was 1.0. The predicted maximal
VO2 was calculated according to the
following formulas, taking into account sex, age, body weight, and
height18,19: for men,
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Follow-up
The end point in this study was the occurrence of SCD, other
causes of death, or heart transplant. SCD was defined as witnessed,
instantaneous collapse leading to death within 1 hour of onset of
symptoms or successful resuscitation from documented
ventricular fibrillation. The coding of the mode of death
was performed by the first author (N.S.) blinded to knowledge of the
patient's exercise BPR and risk factor status. Subsequently, 158
patients were reevaluated at Saint George's Hospital outpatient
clinic, and follow-up data were accumulated until August 1995. Three
patients were followed up elsewhere, and information was obtained from
their physicians.
Statistical Analysis
Data are expressed as mean±SD. Group comparisons were with the
2 test, Fisher's exact test, and
unpaired Student's t test where appropriate. A
two-tailed probability value of <.05 was considered statistically
significant.
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Results |
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All patients completed exercise testing without complication. The principal reason for termination of the exercise was fatigue in 101 patients (63%), shortness of breath in 31 (19%), dizziness and presyncope in 14 (9%), chest pain in 8 (5%), reaching the end of the protocol in 6 (4%), and nonsustained VT in 1. Adequate exercise as evidenced by an RER >1.0 was achieved in all but 17 patients (9 women) in whom RER was between 0.90 and 0.99. The reasons for stopping in these 17 patients were not different from those of the remaining 144 patients.
BP Response
A normal BPR was recorded in 101 patients (63%), and 60
(37%) had an abnormal response. Of these, 27 had a hypotensive
response and 33 a flat response (Table 1
). The two groups achieved a similar
degree of cardiovascular stress as assessed by maximal
predicted heart rate attained (93±10% in the normal BPR group versus
88±12% in the abnormal BPR group, P=NS) (Table 1). Six of
101 patients (6%) with a normal BPR did not reach an RER >1, compared
with 11 of 60 patients (18%) with an abnormal BPR
(P<.001). The percentage predicted
VO2 achieved was higher in the normal
BPR group (73±17% versus 59±18%, P<.001). There
was no difference in the two groups in terms of age (28±8 versus 25±8
years), sex ratio (2.1 versus 1.6), VT on Holter (18% versus 21%),
syncope (24% versus 33%), family history of HCM (34% versus 28%),
family history of HCM and SCD (35% versus 28%), symptoms at the time
of exercise, and echocardiographic left
ventricular dimensions (left ventricular
end-diastolic diameter, 44±6 versus 44±7 mm; left
ventricular end-systolic diameter, 26±6 versus
27±6 mm; maximum left ventricular wall thickness,
21±8 versus 23±9 mm). Left atrial dimension was smaller in
patients with a normal BPR (39±8 versus 43±8 mm;
P<.002) (Table 1).
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Follow-up
The mean follow-up was 44±20 months. The predominant
symptomatic treatment during the period of evaluation was
ß-blockers in 23 patients and verapamil or diltiazem in
17. Thirty-one patients received amiodarone: 7 for sustained
palpitation, 9 for documented recurrent supraventricular
tachyarrhythmias, and 15 who were considered to be at
high risk of sudden death. Two patients underwent myectomy, and 2
received an ICD for nonfatal sudden cardiac arrest (see below). In
addition, dual-chamber pacemakers were implanted in 8 patients: 3 for
recurrent syncope associated with bradycardia and 5 for drug-refractory
obstructive HCM. All these pacemakers were implanted in 1993 to 1994.
The proportion of patients receiving ß-blockers, calcium blockers,
and amiodarone was similar in patients with an abnormal and a
normal BPR (9 versus 14, 7 versus 10, and 13 versus 18,
respectively).
During the follow-up, events occurred in 17 patients (Fig 1).
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SCD occurred in 12 patients: 3 of 101 (3%) in the normal BPR group
compared with 9 of 60 (15%) in the abnormal BPR group
(P<.005; odds ratio, 3). The actuarial survival curve
(Kaplan-Meier) based on the BPR is given in Fig 2. Abnormal BPR had a sensitivity of
75%, a specificity of 66%, a negative predictive value of 97%, and a
positive predictive value of 15% for the prediction of SCD (Table 2).
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Among the 12 patients who experienced sudden cardiac arrest, 2
were successfully resuscitated. The characteristics of these 12
patients as well as the circumstances and possible mechanisms of the
episodes are shown in Table 3. The
patients were young (mean age, 24±7 years; range, 15 to 37 years), and
6 had a family history of HCM and sudden death. Six patients had
experienced syncope before the event, and 3 had nonsustained VT on
48-hour Holter recordings. Three of the 12 episodes of SCD
occurred during or after exercise, and all of the remaining episodes
occurred during moderate daily activities or at rest. Two patients had
documented monomorphic VT (ECG in one, Holter in one) degenerating into
VF. There was no difference in terms of preexisting established risk
factors (ie, syncope, family history of HCM and sudden death,
nonsustained VT on Holter recordings) between these 12 patients
who experienced sudden cardiac arrest or VF and the remaining 149
patients (Table 4).
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Three patients died of other causes: 1 of endocarditis at 24 months, 1 of end-stage heart failure at 2 months, and 1 after mitral valve replacement at 19 months after the exercise test was performed. Two patients underwent orthotopic heart transplantation 24 and 78 months after exercise.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Exercise-related hypotension is a well-recognized feature in patients with HCM. The potential importance of such abnormalities is underlined by the fact that a significant number of SCDs occurred during or after periods of exertion.3,4 We have previously shown in a study of 129 consecutive patients (mean age, 41 years) that exercise-induced hypotension occurred in one third of patients with HCM.13 Exercise-induced hypotension was more common in young patients and was associated with a family history of SCD. Invasive assessment showed that the abnormal BPR during exercise was due to an abnormal peripheral vascular response with an exaggerated decrease in total systemic vascular resistance despite an appropriate rise in cardiac index.13,17 This was associated with reversal of the normal constrictor response seen in nonexercising vascular beds during supine dynamic leg exercise (References 13 and 1713 17 , and G.A. Haywood, MD, unpublished observations). These findings suggest that an abnormal BPR might be important in relation to the genesis of SCD, especially in young patients. Similar observations were reported by another group from Poland.21
This prospective study in the young (average age, 24 years) shows
that an abnormal BPR was associated with an increased risk of SCD that
was independent and not associated with other markers of increased
risk. Risk stratification in HCM remains a major challenge in clinical
management. The incidence of SCD is highest in the young and can be the
first manifestation of the disease. In a study of 78 patients with HCM
who died suddenly, Maron et al4 showed that 89%
were <40 years of age. Fifty-four percent had experienced no
functional limitation before death, and in 43%, SCD was the initial
manifestation of the disease. Data generated from referral centers have
shown that the incidence of SCD is 
2% to 4% per year in adults and
4% to 6% per year in children and
adolescents.22 Although these percentages may be
biased toward more severely ill patients,23
identification of a high-risk cohort has always been a major goal in
the management of patients with HCM, especially those <40 years of
age. However, the mechanisms of SCD are undoubtedly not identical and
may be age-related.
In adults (>25 years old), the single most useful marker of risk for SCD is the finding of episodes of nonsustained VT on Holter monitoring.11,12 Pooled data from two independent studies have shown nonsustained VT on Holter monitoring to have a specificity of 80%, a sensitivity of 69%, and a high negative predictive value (97%) for SCD during 3 years.7 This practical, noninvasive evaluation provides the basis for reassurance for the majority of adults. In the young, however, Holter arrhythmias are uncommon, and the absence of nonsustained VT does not confer safety.24 In addition, other recognized risk factors (syncope, family history of sudden death) do not identify the majority of young patients who die suddenly.
The mechanism by which an abnormal BPR on exercise may lead to SCD remains unclear. Documentation of the initiating mechanisms of SCD in HCM arise from anecdotal reports in which a patient has been fortuitously monitored during an event. Sinus tachycardia, ischemia, and atrial or ventricular tachyarrhythmias have been documented to cause SCD or hemodynamic collapse.2,7,9,25 The hemodynamic consequences of such events may be exaggerated by the concurrent existence of an abnormal vascular pressure response. This could explain the occurrence of SCD during or soon after periods of exertion in some patients.3 Moreover, the evidence suggests that patients with an abnormal BPR have a generalized abnormality of vasomotor control that is likely to be a determinant of risk at rest as well as during exercise. Abnormal exercise BP is strongly associated with an inappropriate increase in renal (G.A. Haywood, unpublished data) and forearm blood flow17 during mild supine leg exercise and with paradoxical forearm vasodilatation during the minor central volume unloading associated with subhypotensive lower-body negative pressure.26 Preliminary evidence reveals unexplained hypotension during daily life activity in >40% of a small cohort of young HCM patients during beat-to-beat ambulatory BP monitoring.27 Regardless of the initiating mechanism, these data led us to propose that altered vascular responses are an important determinant of outcome.
Limitations of the Study
Ideally, the prognostic significance of an abnormal BPR during
exercise would have been assessed in untreated groups; this was not
ethically possible. A similar proportion of normal and abnormal BP
responders received ß-blockers, calcium antagonists, and
amiodarone. There is little reason to suspect that
symptomatic treatment modified risk of SCD. It is important
to emphasize that treatment was not altered on the basis of exercise BP
findings. Whether amiodarone prevented SCD in the 15 patients
who were considered to be at high risk or the 16 patients treated for
arrhythmias is uncertain.28 Thirteen of these 31
patients had an abnormal BPR, and 18 had at least one of the
conventional risk factors; ostensibly, they were a high-risk group. Of
interest, only 1 of the 12 SCD patients was receiving
amiodarone at the time of the event.
Conclusions
An abnormal BPR during exercise has a potential value in the
clinical management of patients with HCM. Its high negative predictive
accuracy in the entire population in the present study allows
reassurance of young patients with a normal BPR. However, the low
positive predictive value probably indicates the high
heterogeneity in the cohort and underlines the
multifactorial mechanisms of SCD in HCM as well as the need for
additional risk stratification.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by grants from the Fédération Française de Cardiologie, Paris, France (N.S.), and the British Heart Foundation (P.M.E.). We gratefully acknowledge Anne O'Donoghue, Shaughan Dickie, Carol Page, and Michele Lee Jones for their technical assistance.
Received November 25, 1996; revision received August 4, 1997; accepted August 11, 1997.
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Writing Committee Members, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Europace, September 1, 2006; 8(9): 746 - 837. [Full Text] [PDF]
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P. M. Elliott, J. R. Gimeno, M. T. Tome, J. Shah, D. Ward, R. Thaman, J. Mogensen, and W. J. McKenna Left ventricular outflow tract obstruction and sudden death risk in patients with hypertrophic cardiomyopathy Eur. Heart J., August 2, 2006; 27(16): 1933 - 1941. [Abstract] [Full Text] [PDF]
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P M Elliott, J R Gimeno, R Thaman, J Shah, D Ward, S Dickie, M T Tome Esteban, and W J McKenna Historical trends in reported survival rates in patients with hypertrophic cardiomyopathy Heart, June 1, 2006; 92(6): 785 - 791. [Abstract] [Full Text] [PDF]
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R. Thaman, P. M. Elliott, J. S. Shah, B. Mist, L. Williams, R. T. Murphy, W. J. McKenna, and M. P. Frenneaux Reversal of Inappropriate Peripheral Vascular Responses in Hypertrophic Cardiomyopathy J. Am. Coll. Cardiol., September 6, 2005; 46(5): 883 - 892. [Abstract] [Full Text] [PDF]
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R. Thaman, J. R. Gimeno, S. Reith, M. T. T. Esteban, G. Limongelli, R. T. Murphy, B. Mist, W. J. McKenna, and P. M. Elliott Progressive left ventricular remodeling in patients with hypertrophic cardiomyopathy and severe left ventricular hypertrophy J. Am. Coll. Cardiol., July 21, 2004; 44(2): 398 - 405. [Abstract] [Full Text] [PDF]
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M. P Frenneaux Assessing the risk of sudden cardiac death in a patient with hypertrophic cardiomyopathy Heart, May 1, 2004; 90(5): 570 - 575. [Full Text] [PDF]
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B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, F. J. Ten Cate, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines J. Am. Coll. Cardiol., November 5, 2003; 42(9): 1687 - 1713. [Full Text] [PDF]
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Writing Committee Members, B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy: A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines Eur. Heart J., November 1, 2003; 24(21): 1965 - 1991. [Full Text] [PDF]
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L. Monserrat, P. M. Elliott, J. R. Gimeno, S. Sharma, M. Penas-Lado, and W. J. McKenna Non-sustained ventricular tachycardia in hypertrophic cardiomyopathy: an independent marker of sudden death risk in young patients J. Am. Coll. Cardiol., September 3, 2003; 42(5): 873 - 879. [Abstract] [Full Text] [PDF]
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M. J. M. Kofflard, F. J. Ten Cate, C. van der Lee, and R. T. van Domburg Hypertrophic cardiomyopathy in a large community-based population: clinical outcome and identification of risk factors for sudden cardiac death and clinical deterioration J. Am. Coll. Cardiol., March 19, 2003; 41(6): 987 - 993. [Abstract] [Full Text] [PDF]
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Q. Ciampi, S. Betocchi, R. Lombardi, F. Manganelli, G. Storto, M. A. Losi, E. Pezzella, F. Finizio, A. Cuocolo, and M. Chiariello Hemodynamic determinants of exercise-induced abnormal blood pressure response in hypertrophic cardiomyopathy J. Am. Coll. Cardiol., July 17, 2002; 40(2): 278 - 284. [Abstract] [Full Text] [PDF]
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 B. J. Maron Hypertrophic Cardiomyopathy: A Systematic Review JAMA, March 13, 2002; 287(10): 1308 - 1320. [Abstract] [Full Text] [PDF]
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W. J McKenna and E. R Behr Hypertrophic cardiomyopathy: management, risk stratification, and prevention of sudden death Heart, February 1, 2002; 87(2): 169 - 176. [Full Text] [PDF]
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 W.J. McKenna, S. Sharma, and P.M. Elliott Management strategies in hypertrophic cardiomyopathy: influence of age and morphology Eur. Heart J. Suppl., October 1, 2001; 3(suppl_L): L10 - L14. [Abstract] [PDF]
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A. M. Varnava, P. M. Elliott, C. Baboonian, F. Davison, M. J. Davies, and W. J. McKenna Hypertrophic Cardiomyopathy: Histopathological Features of Sudden Death in Cardiac Troponin T Disease Circulation, September 18, 2001; 104(12): 1380 - 1384. [Abstract] [Full Text] [PDF]
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S.G. Priori, E. Aliot, C. Blomstrom-Lundqvist, L. Bossaert, G. Breithardt, P. Brugada, A.J. Camm, R. Cappato, S.M. Cobbe, C. Di Mario, et al. Task Force on Sudden Cardiac Death of the European Society of Cardiology Eur. Heart J., August 2, 2001; 22(16): 1374 - 1450. [PDF]
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P. M. Elliott, J. Poloniecki, S. Dickie, S. Sharma, L. Monserrat, A. Varnava, N. G. Mahon, and W. J. McKenna Sudden death in hypertrophic cardiomyopathy: identification of high risk patients J. Am. Coll. Cardiol., December 1, 2000; 36(7): 2212 - 2218. [Abstract] [Full Text] [PDF]
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H. Kokado, M. Shimizu, H. Yoshio, H. Ino, K. Okeie, Y. Emoto, T. Matsuyama, M. Yamaguchi, T. Yasuda, N. Fujino, et al. Clinical Features of Hypertrophic Cardiomyopathy Caused by a Lys183 Deletion Mutation in the Cardiac Troponin I Gene Circulation, August 8, 2000; 102(6): 663 - 669. [Abstract] [Full Text] [PDF]
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M. Guazzi, A. Maltagliati, G. Tamborini, F. Celeste, M. Pepi, M. Muratori, M. Berti, and M. D. Guazzi How the left and right sides of the heart, as well as pulmonary venous drainage, adapt to an increasing degree of head-up tilting in hypertrophic cardiomyopathy: differences from the normal heart J. Am. Coll. Cardiol., July 1, 2000; 36(1): 185 - 193. [Abstract] [Full Text] [PDF]
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 R.C. Saumarez and A.A. Grace Paced ventricular electrogram fractionation and sudden death in hypertrophic cardiomyopathy and other non-coronary heart diseases Cardiovasc Res, July 1, 2000; 47(1): 11 - 22. [Full Text] [PDF]
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 P. Spirito, P. Bellone, K. M. Harris, P. Bernabo, P. Bruzzi, and B. J. Maron Magnitude of Left Ventricular Hypertrophy and Risk of Sudden Death in Hypertrophic Cardiomyopathy N. Engl. J. Med., June 15, 2000; 342(24): 1778 - 1785. [Abstract] [Full Text] [PDF]
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B. J. Maron, W.-K. Shen, M. S. Link, A. E. Epstein, A. K. Almquist, J. P. Daubert, G. H. Bardy, S. Favale, R. F. Rea, G. Boriani, et al. Efficacy of Implantable Cardioverter-Defibrillators for the Prevention of Sudden Death in Patients with Hypertrophic Cardiomyopathy N. Engl. J. Med., February 10, 2000; 342(6): 365 - 373. [Abstract] [Full Text] [PDF]
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M. L. Gil, F. Arribas, and F. G. Cosio Ventricular fibrillation induced by rapid atrial rates in patients with hypertrophic cardiomyopathy Europace, January 1, 2000; 2(4): 327 - 332. [Abstract] [PDF]
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I. Olivotto, B. J. Maron, A. Montereggi, F. Mazzuoli, A. Dolara, and F. Cecchi Prognostic value of systemic blood pressure response during exercise in a community-based patient population with hypertrophic cardiomyopathy J. Am. Coll. Cardiol., June 1, 1999; 33(7): 2044 - 2051. [Abstract] [Full Text] [PDF]
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P. M. Elliott, S. Sharma, A. Varnava, J. Poloniecki, E. Rowland, and W. J. McKenna Survival after cardiac arrest or sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy J. Am. Coll. Cardiol., May 1, 1999; 33(6): 1596 - 1601. [Abstract] [Full Text] [PDF]
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N. Yoshida, H. Ikeda, T. Wada, A. Matsumoto, S. Maki, A. Muro, A. Shibata, and T. Imaizumi Exercise-induced abnormal blood pressure responses are related to subendocardial ischemia in hypertrophic cardiomyopathy J. Am. Coll. Cardiol., December 1, 1998; 32(7): 1938 - 1942. [Abstract] [Full Text] [PDF]
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A. T. Yetman, B. W. McCrindle, C. MacDonald, R. M. Freedom, and R. Gow Myocardial Bridging in Children with Hypertrophic Cardiomyopathy -- A Risk Factor for Sudden Death N. Engl. J. Med., October 22, 1998; 339(17): 1201 - 1209. [Abstract] [Full Text] [PDF]
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K PRASAD and M P FRENNEAUX Sudden death in hypertrophic cardiomyopathy: potential importance of altered autonomic control of vasculature Heart, June 1, 1998; 79(6): 538 - 540. [Full Text]
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K PRASAD and M P FRENNEAUX Hypertrophic cardiomyopathy: is there a role for amiodarone? Heart, April 1, 1998; 79(4): 317 - 318. [Full Text]
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