BMJ 2013;347:f6910 doi: 10.1136/bmj.f6910 (Published 25 November 2013)
Page 1 of 3
Endgames
ENDGAMES CASE REPORT
A patient with hypertrophic cardiomyopathy undergoing non-cardiac surgery 1
Tania C N Elias specialist registrar, geriatric medicine , Judith S L Partridge clinical research fellow, 1 proactive care of older people undergoing surgery (POPS) , Stuart A McCorkell consultant 2 anaesthetist , Jugdeep K Dhesi consultant physician, proactive care of older people undergoing 1 surgery (POPS) Department of Ageing and Health, Guy’s and St Thomas’ NHS Foundation Trust, London SE1 7EH, UK; 2Anaesthetic Department, Guy’s and St Thomas’ NHS Foundation Trust, London, UK 1
A 73 year old woman with hypertension who presented with exertional chest pain was found to have a harsh ejection systolic murmur, with features of left ventricular hypertrophy on electrocardiography. Coronary angiography showed normal coronary arteries and transthoracic echocardiography detected concentric thickening of the left ventricular wall, with hyperdynamic systolic function. These findings were thought to be secondary to hypertension, which was managed with ramipril 10 mg and amlodipine 5 mg. Three years later she returned with breathlessness, and further transthoracic echocardiography suggested severe obstruction of the left ventricular outflow tract owing to systolic anterior motion of the anterior mitral leaflet, with an outflow gradient of up to 160 mm Hg. She was diagnosed with hypertrophic cardiomyopathy and was managed with bisoprolol 5 mg. Her symptoms improved and no arrhythmias were found on 24 hour electrocardiography (figure).
Two years later she developed painful abdominal distension with anaemia. Computed tomography demonstrated bilateral ovarian masses. She was listed for a total abdominal hysterectomy and bilateral salpingo-oophorectomy. The indication for surgery was symptom relief and suspected cancer.
Electrocardiogram with some typical features of hypertrophic cardiomyopathy
Questions 1 What are the pathophysiological changes of hypertrophic cardiomyopathy? 2 What are the clinical features of hypertrophic cardiomyopathy? 3 On the basis of this patient’s clinical history, is her hypertrophic cardiomyopathy likely to be of high or low risk? 4 What risks might hypertrophic cardiomyopathy pose for a patient undergoing non-cardiac surgery? 5 How can these risks be minimised?
Correspondence to: T C N Elias [email protected] For personal use only: See rights and reprints http://www.bmj.com/permissions
Subscribe: http://www.bmj.com/subscribe
BMJ 2013;347:f6910 doi: 10.1136/bmj.f6910 (Published 25 November 2013)
Page 2 of 3
ENDGAMES
Answers
1 What are the pathophysiological changes of hypertrophic cardiomyopathy? Short answer
Hypertrophic cardiomyopathy is an autosomal dominant genetic disorder characterised by left ventricular hypertrophy, impaired diastolic filling, and abnormalities of the mitral valve. These features can cause dynamic obstruction of the left ventricular outflow tract, diastolic dysfunction, myocardial ischaemia, and an increased risk of supraventricular and ventricular tachyarrhythmias.
Long answer
It is thought that a genetic mutation in one of up to 12 sarcomeric and non-sarcomeric proteins causes histological myocyte disarray and fibrosis in hypertrophic cardiomyopathy. Penetrance is variable and phenotypic expression has a broad spectrum. Hypertrophy can occur in any part of the left ventricle, although it is most common in the anterior ventricular septum.1 Obstruction of the left ventricular outflow tract is dynamic, and it is caused by ventricular septal hypertrophy and often systolic anterior motion of the mitral valve apparatus. It may be absent in resting conditions but present at times of increased myocardial contractility or reduced preload or afterload. Impaired myocardial relaxation and diastolic filling can cause diastolic heart failure. Impaired diastolic filling also reduces diastolic coronary artery perfusion, and along with a relative paucity of arterioles to the hypertrophied left ventricle, contributes to myocardial ischaemia. Finally, there is a propensity to both atrial and ventricular arrhythmias; the prevalence of atrial fibrillation was found to be 22% in a large sample of patients with hypertrophic cardiomyopathy from the United States and Italy.2
2 What are the clinical features of hypertrophic cardiomyopathy? Short answer
Most people with hypertrophic cardiomyopathy are asymptomatic, although symptoms may develop at any age.3 Symptoms include exertional chest pain; dyspnoea as a result of heart failure, which may be progressive; palpitations or stroke from arrhythmia; syncope; and sudden death owing to arrhythmias and obstruction of the left ventricular outflow tract. Because obstruction of the left ventricular outflow tract is dynamic, symptoms can be exacerbated during exercise or surgery, which may increase cardiovascular stress or reduce preload or afterload.
Long answer
With the greater availability of echocardiography and genetic screening, more asymptomatic people are being diagnosed as having hypertrophic cardiomyopathy, and the full clinical spectrum of this disease is increasingly recognised. Classic examination findings are a forceful apex beat, with double impulse if the left ventricular outflow tract is obstructed; and a late ejection systolic murmur, which can be augmented by standing or Valsalva manoeuvre and diminished by squatting. Signs of mitral regurgitation may also be present, owing to prolonged systolic anterior motion of the mitral valve. Most patients have an abnormal electrocardiogram, although electrocardiographic features are non-specific and include left ventricular hypertrophy, ST segment changes, and T wave For personal use only: See rights and reprints http://www.bmj.com/permissions
inversion (figure). Electrocardiographic findings do not correlate with clinical outcomes.4 Maximal left ventricular wall thickness is usually greater than 15 mm on transthoracic echocardiography (or ≥2 standard deviations above the mean in children), although this may be segmental, and hypertrophy is almost always asymmetrical.4 Wall thickness may not meet these criteria however in all people with a genetic profile consistent with hypertrophic cardiomyopathy.5
3 On the basis of the patient’s clinical history, is her hypertrophic cardiomyopathy likely to be of high or low risk? Short answer Features such as personal or family history of sudden cardiac death, history of ventricular fibrillation or sustained ventricular tachycardia, recent unexplained syncope, non-sustained ventricular tachycardia, massive maximal left ventricular hypertrophy, and abnormal blood pressure response to exercise convey a greater risk of sudden cardiac death.5 Because our patient first presented with symptoms of left ventricular hypertrophy in her 70s and has no relevant personal or family history, she is probably at low risk of sudden cardiac death or rapidly progressive disease.
Long answer
Although risk stratification is useful to guide management, such as the option of implantable cardioverter defibrillators for primary or secondary prevention, current methods of risk stratification have limitations.5 A considerable proportion of people who die suddenly do not have “high risk” features; it is not clear whether or how multiple risk factors summate to correlate with worse outcomes; and the risk conferred by certain clinical features is not entirely clear from existing evidence. For example, the severity of obstruction of the left ventricular outflow tract is inconsistently associated with a higher incidence of sudden cardiac death, yet this factor correlates with progression of heart failure and death from heart failure and stroke.6
4 What risks might hypertrophic cardiomyopathy pose for a patient undergoing non-cardiac surgery? Short answer The condition is associated with an increased incidence of congestive heart failure, myocardial ischaemia, hypotension, and atrial and ventricular arrhythmias after non-cardiac surgery.7-9 This is probably as a result of worsened left ventricular outflow tract obstruction, diastolic dysfunction, cardiac ischaemia, and risk of arrhythmias. Exacerbating intraoperative and postoperative factors include increased sympathetic discharge during intubation and surgery, as well as reduced preload and afterload from preoperative fluid restriction, fluid and blood loss during surgery, and the effects of anaesthetic and analgesic agents.
Long answer
A retrospective study of 227 patients with hypertrophic cardiomyopathy who underwent non-cardiac surgery in the United States found an odds ratio of 1.61 for death or 2.82 for death or myocardial infarction compared with controls. This was after the results were adjusted for age; sex; race; presence of hypertension and diabetes; and history of coronary artery disease, heart failure, atrial fibrillation, and ventricular Subscribe: http://www.bmj.com/subscribe
BMJ 2013;347:f6910 doi: 10.1136/bmj.f6910 (Published 25 November 2013)
Page 3 of 3
ENDGAMES
arrhythmias.7 However, findings are inconsistent, which might be explained by the relatively low numbers of participants in most studies.7-9 Reliance on a pre-existing diagnosis of hypertrophic cardiomyopathy when selecting participants may also mean that only those with symptomatic and perhaps more severe disease are included, inflating the calculated risks of surgery.7 Indeed, hypertrophic cardiomyopathy is highly heterogeneous, and careful evaluation of a patient’s preoperative exercise tolerance is essential to assess the risks that surgery poses.
5 How can these risks be minimised? Short answer
Intraoperative and postoperative care should aim to minimise excessive catecholamine discharge, which is common during anxiety, intubation, and pain. Preload and afterload should be maintained by minimising both fluid losses and vasodilation through careful choice of anaesthetic and analgesic technique. Close monitoring and minimisation of ventilator pressures are also important.
Long answer
In patients with hypertrophic cardiomyopathy, medical, anaesthetic, and surgical considerations can help minimise the risks of non-cardiac surgery.4 10 Preoperative medical management should include β blockade until and including the morning of surgery, correction of anaemia, avoidance of preoperative dehydration, and use of anxiolytics to avoid excessive catecholamine surges. Intraoperative care should focus on maintenance of preload and afterload. Important elements include arterial monitoring of blood pressure and use of anaesthetics or agents to treat hypotension that have minimal positive chronotropic or inotropic effect (vasoconstrictors are recommended for hypotension that does not respond to fluid therapy5). Caution is needed when using regional or local anaesthesia that may reduce systemic vascular resistance. Fluid and blood loss should be kept to a minimum during surgery, and lung inflation pressures limited when mechanical ventilation is necessary, to prevent a reduction in venous return. It is important to ensure good analgesia and normothermia during the intraoperative and postoperative period to minimise catecholamine discharge. Patients with ongoing fluid losses or haemodynamic instability may be best managed in a critical care unit.
For personal use only: See rights and reprints http://www.bmj.com/permissions
Patient outcome The prevalence of hypertrophic cardiomyopathy is estimated at one in 500.11 The situation described here is therefore a common problem. Knowledge of how best to manage the complexities of these cases before, during, and after surgery is essential to ensure that these patients have the best possible outcomes.
After management of her anaemia, our patient underwent successful total abdominal hysterectomy and bilateral salpingo-oophorectomy. She made a good postoperative recovery, but the masses were found to be metastases from a primary upper gastrointestinal cancer. She had a duodenal stent inserted after developing post-prandial vomiting and is currently undergoing palliative chemotherapy. Competing interests: We have read and understood the BMJ Group policy on declaration of interests and declare the following interests: None. Provenance and peer review: Not commissioned; externally peer reviewed. Patient consent obtained 1 2 3 4 5
6 7 8 9 10 11
Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA 2002;287:1308-20. Olivotto I, Cecchi F, Casey SA, Dolara A, Traverse JH, Maron BJ. Impact of atrial fibrillation on the clinical course of hypertrophic cardiomyopathy. Circulation 2001;104:2517-24. Maron BJ, Casey SA, Poliac LC, Gohman TE, Almquist AK, Aeppli DM. Clinical course of hypertrophic cardiomyopathy in a regional United States cohort. JAMA 1999;281:650-5. Poliac LC, Barron ME, Maron BJ. Hypertrophic cardiomyopathy. Anesthesiology 2006;104:183-92. Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, et al. ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: A report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation 2011;124:2761-96. Maron MS, Olivotto I, Betocchi S, Casey SA, Lesser J, Losi MA, et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med 2003;348:295-303. Hreybe H, Zahid M, Sonel A, Good CB, Shaver J, Saba S. Noncardiac surgery and the risk of death and other cardiovascular events in patients with hypertrophic cardiomyopathy. Clin Cardiol 2006;29:65-8. Haering JM, Comunale ME, Parker RA, Lowenstein E, Douglas PS, Krumholz HM, et al. Cardiac risk of noncardiac surgery in patients with asymmetric septal hypertrophy. Anesthesiology 1996;85:254-9. Kuroiwa M, Arai M, Ueno T, Takenaka T, Okamoto H, Hoka S. Perioperative cardiovascular complications in patients with hypertrophic cardiomyopathy. Masui 2003;52:733-9. Sahoo RK, Sananta KD, Raut PS, Badole UR, Upasani CB. Perioperative anesthetic management of patients with hypertrophic cardiomyopathy for noncardiac surgery: a case series. Ann Cardiac Anaesth 2010;13:253-6. Maron BJ. Hypertrophic cardiomyopathy: an important global disease [editorial]. Am J Med 2004;116:63-5.
Cite this as: BMJ 2013;347:f6910 © BMJ Publishing Group Ltd 2013
Subscribe: http://www.bmj.com/subscribe
Page 1 of 3
Endgames
ENDGAMES CASE REPORT
A patient with hypertrophic cardiomyopathy undergoing non-cardiac surgery 1
Tania C N Elias specialist registrar, geriatric medicine , Judith S L Partridge clinical research fellow, 1 proactive care of older people undergoing surgery (POPS) , Stuart A McCorkell consultant 2 anaesthetist , Jugdeep K Dhesi consultant physician, proactive care of older people undergoing 1 surgery (POPS) Department of Ageing and Health, Guy’s and St Thomas’ NHS Foundation Trust, London SE1 7EH, UK; 2Anaesthetic Department, Guy’s and St Thomas’ NHS Foundation Trust, London, UK 1
A 73 year old woman with hypertension who presented with exertional chest pain was found to have a harsh ejection systolic murmur, with features of left ventricular hypertrophy on electrocardiography. Coronary angiography showed normal coronary arteries and transthoracic echocardiography detected concentric thickening of the left ventricular wall, with hyperdynamic systolic function. These findings were thought to be secondary to hypertension, which was managed with ramipril 10 mg and amlodipine 5 mg. Three years later she returned with breathlessness, and further transthoracic echocardiography suggested severe obstruction of the left ventricular outflow tract owing to systolic anterior motion of the anterior mitral leaflet, with an outflow gradient of up to 160 mm Hg. She was diagnosed with hypertrophic cardiomyopathy and was managed with bisoprolol 5 mg. Her symptoms improved and no arrhythmias were found on 24 hour electrocardiography (figure).
Two years later she developed painful abdominal distension with anaemia. Computed tomography demonstrated bilateral ovarian masses. She was listed for a total abdominal hysterectomy and bilateral salpingo-oophorectomy. The indication for surgery was symptom relief and suspected cancer.
Electrocardiogram with some typical features of hypertrophic cardiomyopathy
Questions 1 What are the pathophysiological changes of hypertrophic cardiomyopathy? 2 What are the clinical features of hypertrophic cardiomyopathy? 3 On the basis of this patient’s clinical history, is her hypertrophic cardiomyopathy likely to be of high or low risk? 4 What risks might hypertrophic cardiomyopathy pose for a patient undergoing non-cardiac surgery? 5 How can these risks be minimised?
Correspondence to: T C N Elias [email protected] For personal use only: See rights and reprints http://www.bmj.com/permissions
Subscribe: http://www.bmj.com/subscribe
BMJ 2013;347:f6910 doi: 10.1136/bmj.f6910 (Published 25 November 2013)
Page 2 of 3
ENDGAMES
Answers
1 What are the pathophysiological changes of hypertrophic cardiomyopathy? Short answer
Hypertrophic cardiomyopathy is an autosomal dominant genetic disorder characterised by left ventricular hypertrophy, impaired diastolic filling, and abnormalities of the mitral valve. These features can cause dynamic obstruction of the left ventricular outflow tract, diastolic dysfunction, myocardial ischaemia, and an increased risk of supraventricular and ventricular tachyarrhythmias.
Long answer
It is thought that a genetic mutation in one of up to 12 sarcomeric and non-sarcomeric proteins causes histological myocyte disarray and fibrosis in hypertrophic cardiomyopathy. Penetrance is variable and phenotypic expression has a broad spectrum. Hypertrophy can occur in any part of the left ventricle, although it is most common in the anterior ventricular septum.1 Obstruction of the left ventricular outflow tract is dynamic, and it is caused by ventricular septal hypertrophy and often systolic anterior motion of the mitral valve apparatus. It may be absent in resting conditions but present at times of increased myocardial contractility or reduced preload or afterload. Impaired myocardial relaxation and diastolic filling can cause diastolic heart failure. Impaired diastolic filling also reduces diastolic coronary artery perfusion, and along with a relative paucity of arterioles to the hypertrophied left ventricle, contributes to myocardial ischaemia. Finally, there is a propensity to both atrial and ventricular arrhythmias; the prevalence of atrial fibrillation was found to be 22% in a large sample of patients with hypertrophic cardiomyopathy from the United States and Italy.2
2 What are the clinical features of hypertrophic cardiomyopathy? Short answer
Most people with hypertrophic cardiomyopathy are asymptomatic, although symptoms may develop at any age.3 Symptoms include exertional chest pain; dyspnoea as a result of heart failure, which may be progressive; palpitations or stroke from arrhythmia; syncope; and sudden death owing to arrhythmias and obstruction of the left ventricular outflow tract. Because obstruction of the left ventricular outflow tract is dynamic, symptoms can be exacerbated during exercise or surgery, which may increase cardiovascular stress or reduce preload or afterload.
Long answer
With the greater availability of echocardiography and genetic screening, more asymptomatic people are being diagnosed as having hypertrophic cardiomyopathy, and the full clinical spectrum of this disease is increasingly recognised. Classic examination findings are a forceful apex beat, with double impulse if the left ventricular outflow tract is obstructed; and a late ejection systolic murmur, which can be augmented by standing or Valsalva manoeuvre and diminished by squatting. Signs of mitral regurgitation may also be present, owing to prolonged systolic anterior motion of the mitral valve. Most patients have an abnormal electrocardiogram, although electrocardiographic features are non-specific and include left ventricular hypertrophy, ST segment changes, and T wave For personal use only: See rights and reprints http://www.bmj.com/permissions
inversion (figure). Electrocardiographic findings do not correlate with clinical outcomes.4 Maximal left ventricular wall thickness is usually greater than 15 mm on transthoracic echocardiography (or ≥2 standard deviations above the mean in children), although this may be segmental, and hypertrophy is almost always asymmetrical.4 Wall thickness may not meet these criteria however in all people with a genetic profile consistent with hypertrophic cardiomyopathy.5
3 On the basis of the patient’s clinical history, is her hypertrophic cardiomyopathy likely to be of high or low risk? Short answer Features such as personal or family history of sudden cardiac death, history of ventricular fibrillation or sustained ventricular tachycardia, recent unexplained syncope, non-sustained ventricular tachycardia, massive maximal left ventricular hypertrophy, and abnormal blood pressure response to exercise convey a greater risk of sudden cardiac death.5 Because our patient first presented with symptoms of left ventricular hypertrophy in her 70s and has no relevant personal or family history, she is probably at low risk of sudden cardiac death or rapidly progressive disease.
Long answer
Although risk stratification is useful to guide management, such as the option of implantable cardioverter defibrillators for primary or secondary prevention, current methods of risk stratification have limitations.5 A considerable proportion of people who die suddenly do not have “high risk” features; it is not clear whether or how multiple risk factors summate to correlate with worse outcomes; and the risk conferred by certain clinical features is not entirely clear from existing evidence. For example, the severity of obstruction of the left ventricular outflow tract is inconsistently associated with a higher incidence of sudden cardiac death, yet this factor correlates with progression of heart failure and death from heart failure and stroke.6
4 What risks might hypertrophic cardiomyopathy pose for a patient undergoing non-cardiac surgery? Short answer The condition is associated with an increased incidence of congestive heart failure, myocardial ischaemia, hypotension, and atrial and ventricular arrhythmias after non-cardiac surgery.7-9 This is probably as a result of worsened left ventricular outflow tract obstruction, diastolic dysfunction, cardiac ischaemia, and risk of arrhythmias. Exacerbating intraoperative and postoperative factors include increased sympathetic discharge during intubation and surgery, as well as reduced preload and afterload from preoperative fluid restriction, fluid and blood loss during surgery, and the effects of anaesthetic and analgesic agents.
Long answer
A retrospective study of 227 patients with hypertrophic cardiomyopathy who underwent non-cardiac surgery in the United States found an odds ratio of 1.61 for death or 2.82 for death or myocardial infarction compared with controls. This was after the results were adjusted for age; sex; race; presence of hypertension and diabetes; and history of coronary artery disease, heart failure, atrial fibrillation, and ventricular Subscribe: http://www.bmj.com/subscribe
BMJ 2013;347:f6910 doi: 10.1136/bmj.f6910 (Published 25 November 2013)
Page 3 of 3
ENDGAMES
arrhythmias.7 However, findings are inconsistent, which might be explained by the relatively low numbers of participants in most studies.7-9 Reliance on a pre-existing diagnosis of hypertrophic cardiomyopathy when selecting participants may also mean that only those with symptomatic and perhaps more severe disease are included, inflating the calculated risks of surgery.7 Indeed, hypertrophic cardiomyopathy is highly heterogeneous, and careful evaluation of a patient’s preoperative exercise tolerance is essential to assess the risks that surgery poses.
5 How can these risks be minimised? Short answer
Intraoperative and postoperative care should aim to minimise excessive catecholamine discharge, which is common during anxiety, intubation, and pain. Preload and afterload should be maintained by minimising both fluid losses and vasodilation through careful choice of anaesthetic and analgesic technique. Close monitoring and minimisation of ventilator pressures are also important.
Long answer
In patients with hypertrophic cardiomyopathy, medical, anaesthetic, and surgical considerations can help minimise the risks of non-cardiac surgery.4 10 Preoperative medical management should include β blockade until and including the morning of surgery, correction of anaemia, avoidance of preoperative dehydration, and use of anxiolytics to avoid excessive catecholamine surges. Intraoperative care should focus on maintenance of preload and afterload. Important elements include arterial monitoring of blood pressure and use of anaesthetics or agents to treat hypotension that have minimal positive chronotropic or inotropic effect (vasoconstrictors are recommended for hypotension that does not respond to fluid therapy5). Caution is needed when using regional or local anaesthesia that may reduce systemic vascular resistance. Fluid and blood loss should be kept to a minimum during surgery, and lung inflation pressures limited when mechanical ventilation is necessary, to prevent a reduction in venous return. It is important to ensure good analgesia and normothermia during the intraoperative and postoperative period to minimise catecholamine discharge. Patients with ongoing fluid losses or haemodynamic instability may be best managed in a critical care unit.
For personal use only: See rights and reprints http://www.bmj.com/permissions
Patient outcome The prevalence of hypertrophic cardiomyopathy is estimated at one in 500.11 The situation described here is therefore a common problem. Knowledge of how best to manage the complexities of these cases before, during, and after surgery is essential to ensure that these patients have the best possible outcomes.
After management of her anaemia, our patient underwent successful total abdominal hysterectomy and bilateral salpingo-oophorectomy. She made a good postoperative recovery, but the masses were found to be metastases from a primary upper gastrointestinal cancer. She had a duodenal stent inserted after developing post-prandial vomiting and is currently undergoing palliative chemotherapy. Competing interests: We have read and understood the BMJ Group policy on declaration of interests and declare the following interests: None. Provenance and peer review: Not commissioned; externally peer reviewed. Patient consent obtained 1 2 3 4 5
6 7 8 9 10 11
Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA 2002;287:1308-20. Olivotto I, Cecchi F, Casey SA, Dolara A, Traverse JH, Maron BJ. Impact of atrial fibrillation on the clinical course of hypertrophic cardiomyopathy. Circulation 2001;104:2517-24. Maron BJ, Casey SA, Poliac LC, Gohman TE, Almquist AK, Aeppli DM. Clinical course of hypertrophic cardiomyopathy in a regional United States cohort. JAMA 1999;281:650-5. Poliac LC, Barron ME, Maron BJ. Hypertrophic cardiomyopathy. Anesthesiology 2006;104:183-92. Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, et al. ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: A report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation 2011;124:2761-96. Maron MS, Olivotto I, Betocchi S, Casey SA, Lesser J, Losi MA, et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med 2003;348:295-303. Hreybe H, Zahid M, Sonel A, Good CB, Shaver J, Saba S. Noncardiac surgery and the risk of death and other cardiovascular events in patients with hypertrophic cardiomyopathy. Clin Cardiol 2006;29:65-8. Haering JM, Comunale ME, Parker RA, Lowenstein E, Douglas PS, Krumholz HM, et al. Cardiac risk of noncardiac surgery in patients with asymmetric septal hypertrophy. Anesthesiology 1996;85:254-9. Kuroiwa M, Arai M, Ueno T, Takenaka T, Okamoto H, Hoka S. Perioperative cardiovascular complications in patients with hypertrophic cardiomyopathy. Masui 2003;52:733-9. Sahoo RK, Sananta KD, Raut PS, Badole UR, Upasani CB. Perioperative anesthetic management of patients with hypertrophic cardiomyopathy for noncardiac surgery: a case series. Ann Cardiac Anaesth 2010;13:253-6. Maron BJ. Hypertrophic cardiomyopathy: an important global disease [editorial]. Am J Med 2004;116:63-5.
Cite this as: BMJ 2013;347:f6910 © BMJ Publishing Group Ltd 2013
Subscribe: http://www.bmj.com/subscribe
