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Table of Contents
Year : 2014  |  Volume : 17  |  Issue : 3  |  Page : 211-221
Hypertrophic cardiomyopathy part II - Anesthetic and surgical considerations

1 Department of Cardiac Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
2 Department of Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
3 Department of Anaesthesiology, All India Institute of Medical Sciences Raipur, Chhattisgarh, India

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Date of Submission18-Apr-2014
Date of Acceptance27-May-2014
Date of Web Publication3-Jul-2014


Hypertrophic cardiomyopathy (HCM) poses many unique challenges regarding the conduct of anesthesia and surgery. Adequate preload, control of sympathetic stimulation, heart rate, and increased afterload are required to decrease the left ventricular outflow tract obstruction. Comprehensive intraoperative transesophageal echocardiography (TEE) examination confirms the diagnosis, elucidates the pathophysiology, and identifies the various anomalies of mitral valve apparatus and allows assessment of the adequacy of surgery. In this review, we focus on the preoperative assessment, conduct of anesthesia and comprehensive TEE examination of patients presenting for surgery with HCM. The various surgical options are extended myectomy and resection, plication and release.

Keywords: Anesthesia; Hypertrophic cardiomyopathy; Myectomy; Transesophageal echocardiography

How to cite this article:
Varma PK, Raman SP, Neema PK. Hypertrophic cardiomyopathy part II - Anesthetic and surgical considerations. Ann Card Anaesth 2014;17:211-21

How to cite this URL:
Varma PK, Raman SP, Neema PK. Hypertrophic cardiomyopathy part II - Anesthetic and surgical considerations. Ann Card Anaesth [serial online] 2014 [cited 2021 Dec 7];17:211-21. Available from:

   Introduction Top

Cleland [1] in Hammersmith Hospital, London performed the first surgery for hypertrophic cardiomyopathy (HCM). It consisted of a simple incision in the prominent muscular ridge in the septum (myotomy). Morrow et al. [2],[3] pioneered the surgical therapy for HCM. His procedure: Surgical myectomy became the gold standard for treatment of HCM patients with left ventricular outflow tract obstruction (LVOTO). Other surgical procedures were also described and include left atrial approach for septal myectomy; right ventricular approach with thinning of the ventricular septum, mitral valve replacement, modified Konno's procedure, and left ventricular (LV) apicoaortic conduit. Recently, minimally invasive left atrial approach for septal myectomy was described by Mohr et al. [4] Earlier, we had reviewed the pathology and pathophysiology of HCM and indications for surgery. [5]

Preoperative workup

The aim of preoperative evaluation is to identify patients with obstructive physiology and patients likely to develop obstruction on provocation, optimize cardiac function and prepare an appropriate intraoperative and postoperative plan for monitoring and management. [6] Dyspnea due to diastolic dysfunction, and syncope and presyncope due to LVOTO occur in symptomatic patients. Angina may occur in the absence of coronary artery disease and is due to myocardial oxygen supply-demand imbalance, diastolic abnormalities, and abnormal coronary vasodilation. [7] History should include previous episodes of arrhythmia, requiring treatment. Characteristic murmur of HCM is heard on the left sternal border and does not radiate to carotids and is worsened by conditions that decrease preload. [8] The chest X-ray may be normal, or the heart shadow may be slightly enlarged. Features of left atrial enlargement may be present. The electrocardiography (ECG) abnormalities include increased QRS voltages, left axis deviation, left ventricular hypertrophy (LVH), and ST-T abnormalities. There is poor correlation between the ECG voltages and the extent of LVH seen on echocardiography. [9] Transthoracic echocardiography (TTE) is the primary modality for screening and diagnosis of HCM. [9] Comprehensive TTE should document the points shown in [Table 1]. [10] Cardiac magnetic resonance imaging (MRI) [Figure 1] is recommended when TTE findings are equivocal and is very useful for quantification of myocardial fibrosis seen as late gadolinium enhancement. [10],[11] Nuclear studies and positron emission tomography are currently used only as experimental tools. [10],[11] Patients identified for corrective procedure undergo hemodynamic assessment [Table 2]. Left ventricular end-diastolic pressure (LVEDP) provides an idea of the coronary perfusion pressure that must be maintained in these patients in the perioperative period. Coronary angiogram is indicated in patients with angina and intermediate and high-risk for coronary artery disease. [9]
Figure 1: (a) Four-chamber end-diastolic cardiac magnetic resonance (CMR) image of a 27-year-old asymptomatic patient with hypertrophic cardiomyopathy (HCM) with predominately ventricular septal hypertrophy (maximal wall thickness, 24 mm). (b) Four-chamber end-diastolic CMR image in a 16-year-old patient demonstrates increased left ventricular wall thickness confined to the apex (asterisks), consistent with a diagnosis of apical HCM. CMR is increasingly used to delineate all the phenotypic expressions of HCM. LA: Left atrium; RV: Right ventricle; VS: Interventricular septum; CMR: Cardiac MRI" Reprinted from Nagueh et al.[10] with permission from Elsevier Inc

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Table 1: Transthoracic echocardiography assessment[10]

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Table 2: Hemodynamic data in HCM

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   Anesthesia considerations Top

Patients with HCM are treated with β-blockers, calcium channel blockers, amiodarone, disopyramide; these drugs should be continued through the perioperative period. It may be prudent to start metoprolol in patients not receiving any cardiac medications. Metoprolol is titrated to a heart rate of 60-65 beats/min, which is considered a marker of adequate dosing. [6],[9] β-blockers reduce the heart rate and LV contractility, both of which are beneficial for reducing the LVOTO. The preoperative anxiety is controlled with benzodiazepines and/or opioids. Premedication with glycopyrrolate and atropine is avoided because of tachycardia. In patients with atrial fibrillation, oral anticoagulant should be converted to heparin in the perioperative period. Prolonged perioperative fasting and dehydration should be avoided; the reduction in preload, which is exacerbated with anesthesia induction, will worsen the LVOTO. The hypertrophic noncompliant myocardium is very sensitive to ischemia; hence, adequate coronary perfusion pressure should be maintained. A controlled heart rate and sinus rhythm are very much desirable because the hypertrophied and poorly complaint LV requires timed atrial "kick" for effective filling. Consequently, preservation of preload and afterload, controlled heart rate, sinus rhythm, mild suppression of myocardial contractility, and maintenance of myocardial perfusion pressure are the goals of anesthetic management.

Intraoperative monitoring

Invasive arterial blood pressure must be continuously monitored as hypotension is poorly tolerated by these patients. The central venous pressure poorly reflects the left sided filling pressures due to reduced LV compliance. Pulmonary capillary wedge pressure is usually less than the measured LVEDP due to diastolic dysfunction associated with LV hypertrophy. The peak "a" wave pressure of the pulmonary capillary wedge pressure trace represents the best estimate of LVEDP in the presence of diastolic dysfunction. [11] Pulmonary artery catheter placement has been associated with arrhythmias that may adversely affect hemodynamics. [6] Its routine use is not necessary in view of the risks associated with its placement and its limited diagnostic utility. [6],[8]

Conduct of anesthesia

In patients of HCM, increased myocardial contractility, decreased preload and afterload, exacerbate the degree of LVOTO. Anesthetic induction should be performed carefully by titration of induction agents to avoid hypotension as well as sympathetic activation. Either propofol or thiopentone sodium can be used; both have myocardial depressant properties and can lower the afterload. Etomidate has little untoward effect on the cardiovascular system and is an attractive option provided sympathetic ablation is provided by adequate doses of opioids. [12] Any decrease in blood pressure should be treated by judicious preloading and by increasing the afterload. Use of α1-adrenergic agonists such as phenylephrine increases the systemic vascular resistance (SVR) and decreases the LVOTO. [6],[10],[13] β-adrenergic agents, dopamine, dobutamine, epinephrine or isoproterenol, worsen LVOTO due to their positive inotropic and chronotropic effects. [6],[13] It is important not to inactivate an implanted DDD pacemaker during anesthesia when it has been placed for timed atrial contraction and gradient reduction. [14] Tachycardia associated with direct laryngoscopy and intubation can be prevented by pretreatment with intravenous metoprolol or esmolol. This practice is recommended, especially in patients with history of heart failure symptoms, angina, or HCM-related syncope or high resting gradients. [6] It is important to choose a muscle relaxant without histamine releasing (atracurium) and vagolytic (pancuronium) properties. Vecuronium is well-suited for this purpose as it produces a desirable decrease in heart rate when combined with opioids; however, one should consider basal heart rate before selecting a muscle relaxant. Cardiac arrest has been reported with vecuronium in patients receiving β-blocker and opioids. Sevoflurane is better suited for the maintenance of anesthesia than isoflurane or desflurane as it has minimal effect on heart-rate and SVR. [6],[13] Volatile agents may cause atrioventricular block and depress myocardial function in patients who are on verapamil. [15] Although nitrous oxide use is reported in HCM patients, [16] it is not preferred because of sympathetic stimulation and possibility of increase in the pulmonary vascular resistance. [13] Dexmedetomidine is useful as it reduces the heart rate and blocks the sympathetic stimulation, [15] however boluses can lead to hypotension. Mechanical ventilation with high tidal volume and positive end expiratory pressure are unsuited due to the reduction in the preload, which provokes LVOTO. [13] The anticipated sympathetic stimulation during surgical incision, sternotomy, etc., should be controlled by opioids and volatile agents. In case of development of atrial fibrillation, early synchronized cardioversion is the treatment of choice. [13] Pharmacologic correction of atrial fibrillation with amiodarone is inappropriate as its action takes time and its bolus is associated with hypotension. [17],[18] These patients can also develop other arrhythmia such as brady-arrhythmia, supraventricular tachycardia, ventricular tachycardia or ventricular fibrillation [13] for which appropriate pharmacologic agent and/or defibrillation should be kept ready.

   Anesthesia for noncardiac surgery Top

In general, all considerations mentioned above apply. However, the management of a parturient patient with HCM presents several unique challenges. Several hemodynamic changes occur during various trimesters and stages of delivery. The major hemodynamic changes during pregnancy are decreased SVR, an increase in blood volume, and aortocaval compression during later stages of pregnancy. Increased blood volume can offset aggravating LVOTO effect of decreased SVR. The effect of aortocaval compression is variable depending on their effects on preload and afterload. Uterine contraction of labor increases preload and afterload, increased preload and afterload are beneficial for LVOTO, but has potential to precipitate pulmonary edema by increasing the LVEDP. Patients with obstructive physiology poorly tolerate the Valsalva maneuvers associated with the second stage of labor. [19] Major blood loss during labor can aggravate LVOTO by decreasing preload and reflex tachycardia. In the immediate post-delivery period, there is auto-transfusion of uterine blood and a rapid increase in peripheral vascular resistance due to involution of the uterus. Overzealous fluid resuscitation to replace blood loss of labor can lead to pulmonary edema during this phase. [6],[19] Both ergometrine and oxytocin induce uterine contraction. The uterine contraction-induced by oxytocin can increase the central blood volume by 10-25%. [20] The actions of ergometrine and oxytocin on SVR are different. Oxytocin reduces the SVR and increases the heart rate, whereas ergometrine increases the SVR and appears beneficial for these patients. The risk of death during pregnancy is increased in patients with HCM and LVOT obstruction. Therefore, the patients with obstructive physiology should be identified, and their risk of sudden cardiac death should be evaluated. Asymptomatic HCM patients can be reassured about their pregnancy. [21] Patients with HCM benefit from labor analgesia and active intervention during labor. For the hypotensive patient, resuscitation should be done with fluids and phenylephrine. Left lateral decubitus position mitigates the inferior vena-caval compression from the gravid uterus. Inotropes and vasodilators are avoided. The second stage of labor should be preferably cut short by a planned instrumental delivery under labor analgesia. [6],[19] Patients undergoing cesarean section need careful anesthetic evaluation. Because of the vasodilatation associated with sympathetic blockade, regional anesthesia may lead to critical reduction of preload and afterload and precipitate LVOTO in these patients. However, the safety of neuraxial blockade has been documented in two large case series of pregnant patients with HCM some of whom required anesthesia for labor. [21],[22] Epidurals have been employed in patients with significant LVOT gradient ("florid disease"). There was no maternal or fetal morbidity from neuraxial blockade. [23] When local anesthetics are employed, dilute solutions are better and boluses should be administered in fractional doses. [22] Isobaric bupivacaine has been used intrathecally for cesarean [24] and epidural boluses of 0.25% bupivacaine have been administered without event. [25] Ropivacaine should be considered the local anesthetic of choice because it is more cardio-stable than bupivacaine and has longer onset time than lignocaine. The longer the onset time, gentler the onset of sympathetic blockade from neuraxial blockade. [22] There is no risk of adverse hemodynamic changes from administration of intrathecal or epidural opioid and hence can be safely employed for non-cardiac surgery.

The use of pneumo-peritoneum for laparoscopic surgery requires special mention. The cardiovascular effects of pneumo-peritoneum are due to the effects of hypercarbia and elevated intraabdominal pressure. The combined effect is to produce sympathetic stimulation and an acute decrease in venous return, which is poorly tolerated by patients with HCM. Intraabdominal pressure should be carefully monitored and maintained below 15 mm Hg, and the duration of pneumo-peritoneum should be kept short. [26] Transesophageal echocardiography (TEE) during non-cardiac surgery is an evolving area and appears useful in symptomatic patients with diagnosed HCM and in those patients in whom hemodynamic status deterioration is not corrected with the usual resuscitative measures. [27]

Intraoperative Transesophageal Echocardiography [Table 1]

Two-dimensional TEE assessment

Confirmation of diagnosis

Hypertrophic cardiomyopathy is usually diagnosed when the LV wall thickness exceed >15 mm in any myocardial segment without any other apparent cause. [5] The symptomatic patients have septal wall thickness exceeding 20 mm. The typical pattern of ventricular thickening is asymmetric hypertrophy rather than uniform concentric hypertrophy and usually involves the basal and mid anterior wall. [5] The involvement of basal septum can be appreciated in the mid-esophageal (ME) 5-chamber view or ME long-axis view (MELAX). The LVH and the wall thickness can also be assessed in the trans-gastric (TG) short axis views; [28] the LV walls are greatly hypertrophied and there is near obliteration of the ventricular cavity during systole. The inferolateral wall (formerly called the posterior wall) thickness is also measured in this view. A ratio of the septal wall to the inferolateral wall thickness >1.3 is suggestive of asymmetric septal hypertrophy in nonhypertensive individuals. In hypertensive individuals this ratio must be >1.5 for the diagnosis of asymmetric hypertrophy. [29] The various patterns of LVH in HCM and differentiation from sigmoid septal bulge seen in elderly patients are described in part 1 of the review. [5] Tissue Doppler imaging (TDI) will identify reduced systolic (S) and diastolic (e') velocity; this reduction in velocities may occur even before the onset of significant hypertrophy. [10],[30] The reduced systolic velocity in the presence of a normal or elevated ejection fraction is suggestive of HCM. Mitral annular systolic velocity <4 m/s is an independent predictor of heart failure and death. [31] Strain rate imaging is another tool to differentiate the hypertrophy of HCM from that of hypertension. In HCM, the longitudinal strain and the radial strain are markedly reduced. [32] The LV ejection fraction is usually normal or increased and can be measured using the Simpsons' method in the ME four-chamber view or the ME two-chamber view.

Left ventricular outflow tract obstruction assessment

The point of LVOTO [33] is determined by the point where the anterior mitral leaflet (AML) contacts the hypertrophied septum [Figure 2]. This can be determined by 2D color mapping, continuous wave Doppler (CWD) and sequential interrogation of the gradient by pulse wave Doppler (PWD). [10],[31],[34] The myectomy is extended below the point of LVOTO to allow the blood flow to track away from the mitral valve. The MELAX view should be used to determine the extent of the resection. The transverse thickness of the proximal and mid-septum determines the depth of septal resection at both levels. The myectomy should be sufficiently thick and also should extend to at least 1.5 cm below the mitral-septal contact point, often to the base of papillary muscles to redirect the flow anteriorly and prevent systolic anterior motion (SAM) [Figure 3]a and b. Resection is not done medially in the proximal anterior septum as this region is not involved in the formation of LVOTO. Moreover, resection in this area can lead to ventricular septal defect and conduction blocks. [33]
Figure 2: "Transesophageal echocardiography of septal measurements before myectomy (left) (thickness, 2.9 cm) and after myectomy (right) (thickness, 1.5 cm). The myectomy should extend beyond septomitral contact".[10] If the sub-aortic septum is resected only down to the tips of the mitral leaflets, flow is still redirected by the remaining septal bulge so that it comes from a posterior direction leading to persistent systolic anterior motion and obstruction.[59] The proximal incision should be placed away from the aortic annulus to prevent development of AI. LA: Left atrium; RV: Right ventricle; AI: Aortic insufficiency (reprinted with permission from Nagueh et al.[10] from Elsevier Inc.)

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Figure 3: (a) "Early in systole, flow drag is the dominant hydrodynamic force on the mitral leafl ets. After the mitral-septal contact, the pressure difference (gradient) is the force that pushes the mitral leaflet further into the septum". (b) The prominent midseptal bulge redirects outflow so that it comes from a relatively posterior direction, catching the anteriorly positioned mitral valve and pushing it into the septum. After extended myectomy, flow tracks more anteriorly and medially, away from the mitral leafl ets (reprinted with permission from Sherrid and Arabadjian[33] from Elsevier Inc.)

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Color flow Doppler assessment

The interventricular septum, SAM and mitral regurgitation (MR) jet in mid-systole are examined in MELAX view. The color flow mapping in this view should include the LV cavity to the outflow tract so that the region of aliasing can be noted. In HCM, flow acceleration occurs in the mid-ventricle; therefore, the aliasing begins just below the site of the obstruction with the color mosaic worsening in the LV outflow tract (LVOT). A posteriorly directed MR jet is also seen in this view. These color signals often combine to form the appearance of the letter "Y". The descending limb of the "Y" is formed by the flow acceleration below the LVOT; the MR jet and the color aliasing in the LVOT form the other two limbs. [32] The point of flow acceleration and aliasing has important implications in planning the myectomy.

Doppler assessment

Continuous wave Doppler and PWD help identifying the presence, location and severity of LVOT gradient. The Deep trans-gastric long axis (DTGLAX) and/or the trans-gastric long axis (TGLAX) views are utilized for assessing the Doppler gradients. The MELAX and the ME 5-chamber view do not provide Doppler alignment and should not be used for assessing gradients. The CWD reveals the maximum gradient across the LVOT. In HCM, the obstruction is variable and characterized by a progressive decrease in orifice size and increasing velocity and acceleration across the progressively narrowing orifice; however, blood continues to be ejected even after attaining the peak Doppler velocity. [33],[35] The flow pattern leads to a peak after mid-systole and the characteristic leftward concavity of the ascending limb in HCM. [33],[35] The Doppler trace of obstructive HCM has a "dagger" shaped configuration. The CWD trace has an "inflection point" on the ascending limb followed by concavity to the left before peaking after mid-systole. This inflection point occurs between a velocity of 1-2.5 m/s. This inflection point coincides with the point where mitral-septal contact occurs [33],[36] [Figure 4]. The other causes of the LVOT gradient includes sub-aortic membrane, aortic stenosis and another entity called the "complete systolic emptying". [37] In the first two conditions, the LVOT CWD trace is symmetrical, and bell shaped without the leftward concavity. Care should be taken to distinguish the CWD trace of LVOTO from that of MR. The shape of the MR Doppler trace tends to be more rounded and symmetric [Figure 5]. Complete systolic emptying is a condition that occurs in a hypertrophic, nonobstructed and vigorously contracting LV. [36] The CWD trace in complete systolic emptying is different from that of HCM. There is no mitral-septal contact and hence the trace does not show inflection point and once the velocity reaches the peak, there is no ejection of blood into the aorta, and hence the velocity abruptly drops to zero. The gradient measured by CWD can be confirmed by taking an intraoperative needle pressure gradient between the LV and aorta. [34] The PWD is used to sequentially interrogate the area between the LV apex and the LVOT to define the anatomical level of the obstruction. The PWD and the CFD together help in pinpointing the site of the gradient. [34] Another PWD pattern observed in obstructive HCM is the 'lobster claw" abnormality obtained at the entrance of LVOT, upstream to the mitral-septal contact, in the body of the LV [35] [Figure 6].
Figure 4: In aortic stenosis, as velocity increases, acceleration decreases. In contrast, in obstructive hypertrophic cardiomyopathy (HCM), as velocity increases, acceleration also increases. In obstructive HCM, the rising pressure difference forces the mitral leaflet against the septum, which decreases the orifice size and further increases the pressure difference. Progressive orifice narrowing also explains why the jet peaks late in systole in obstructive HCM. Arrow points to the inflection point (reprinted with permission from Sherrid et al.[35] from Elsevier Inc.)

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Figure 5: Continuous-wave (CW) Doppler recordings of peak velocity across the left ventricular outflow tract (LVOT) (cross: 4.5 m/s) (left) and peak velocity of mitral regurgitation signal (arrow: 6.3 m/s) (right). The concave-to-the-left contour of the Doppler CW jet causes a decrease in the LVOT orifice size as systole progresses and as the mitral valve is pushed further into the septum. Identification of this contour can be useful to differentiate high CW jets of dynamic LVOT obstruction from mitral regurgitation and from valvular aortic stenosis (reprinted with permission from Nagueh et al.[10] from Elsevier Inc.)

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Figure 6: Pulse wave Doppler recording of at the entrance of left ventricular outflow tract (LVOT) showing abrupt decrease in velocities giving the appearance of "lobster claw". The nadir of the drop times exactly with the peak of the gradient in LVOT because the drop is caused by afterload mismatch due to mitroseptal contact. The left ventricle is unable to maintain instantaneous ejection against the sudden rise in afterload (reprinted from Sherrid et al.[35] with permission from Elsevier)

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Assessment of mitral valve

Understanding the mechanics of the mitral-septal contact is important in individualizing the repair for each patient. There are a number of structural abnormalities of the mitral valve in HCM that contribute to the overlap of the inflow and outflow portions of the LV. [5] These factors lead to a coaptation between the bodies of the two leaflets rather than the leaflet tips. [33],[38] Mostly, it is the AML that makes contact with the septum. Rarely, it is the posterior mitral leaflet (PML) that extends beyond the coaptation point and obstructs the LVOT. [39] The slack mitral valve is swept into the LVOT towards the hypertrophied basal septum because of the "drag force" developed with the LV ejection [Figure 3]a. The longer the mitral valve stays in contact with the septum, the higher the gradient. [33] The measurement of the AML and PML length is crucial. The MELAX view or the 5-chamber view can be used for measurement of the leaflet lengths. The AML length is measured from its tip to the insertion of the noncoronary cusp of the aortic valve. Though this measurement includes inter-valvar septum, this measurement has been advocated because it is highly reproducible. Patients with AML length >33 mm are likely candidates for horizontal AML plication. Leaflet calcification should be excluded as it contraindicates this type of repair. Patients with AML length >40 mm may require resection of the terminal portion of the AML or may require an Alfieri type of repair. [33],[40] The mismatch between the AML and PML can be quantified by measuring the coaptation zone between the two leaflets. [10] The coaptation zone between the leaflets is best seen in the DTGLAX view.

The papillary muscles are usually hypertrophied; additionally, 13% patients with HCM have abnormal insertion of papillary muscles. Anomalous insertion of papillary muscles occurs when one or both heads of papillary muscles insert into the ventricular aspect of the tip, mid or base of the AML or rarely into the sub-aortic septum. These attachments occur without intervening chordae tendinae. In addition, there may be chordal attachments that connect the AML to the lateral LV wall. The net effect of these abnormal attachments is to draw the mitral valve into the LVOT and contribute to the LVOTO. Failure to detect and address this issue during surgery leads to unrelieved gradients after surgery. [33],[40] The TG two-chamber view is ideal for studying the papillary muscle thickness and insertion. These findings should be supplemented with the information from the ME 5-chamber and the MELAX views. Particular care must be taken to exclude antero-apical displacement of anterolateral papillary muscle, shorter inter-papillary distance, double bifid papillary muscle, direct papillary muscle attachment to mitral valve without chordae, aberrant papillary muscle and hypermobile anterolateral papillary muscles. Anomalous insertion of papillary muscles should be carefully looked for especially when the gradients are high and septal wall thickness is <18 mm. During the surgery, the anomalous portions of the papillary muscles are thinned or resected. If the papillary muscles inserts only into the mid or base of the AML and not into the tips of AML, then they can be safely resected. [33],[40]

Mitral regurgitation

Systolic anterior motion causes a gap in the coaptation of leaflets (inter-leaflet gap). The gap is created between the leaflets because of the failure of the PML to move toward the outflow tract as much as the AML. The gap directs the MR jet laterally and posteriorly and occurs during mid and late systole. This finding is highly suggestive of an obstructive HCM. The MR in HCM is a secondary phenomenon. [5],[10],[11] If the MR jet is directed anteriorly, or toward the center, then other causes of MR should be sought such as mitral valve prolapse, ruptured chordae, chordal elongation or thickening and infective endocarditis. [5],[41] The severity of MR in dynamic obstruction varies with the severity of LVOTO; an increase in LVOTO causes an increase in severity of MR. [10]

Assessment of diastolic function

There is poor correlation between the LVEDP measured invasively and estimated by the E/A ratio, E wave deceleration time of the mitral inflow velocities and the pulmonary venous velocities. There is modest correlation between the E/e' ratio derived from TDI of the lateral mitral annulus to the LVEDP. [42] The TDI of the lateral mitral annulus reveals markedly reduced e' and a' velocity when the LVEDP is elevated. When the LVEDP is > 20 mmHg, the E/e' ratio is markedly elevated [Figure 7]a and b. [10] The flow propagation velocity measured from a color M mode of the mitral inflow shows a reduced slope. [33] Another clue to diastolic function is the left atrial size. If the left atrial size is normal, then the left atrial pressure and the LVEDP are likely normal. [43] Left atrial volume indexed to body surface area should be assessed to get a true estimate of the left atrial size. [10] Patients with HCM who have a normal left atrial volume of ≤28 cm 3 /m 2 have normal LV filling pressures. [43]
Figure 7:

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Post cardiopulmonary bypass assessment

Transesophageal echocardiography is used to assess the adequacy of repair and detect postoperative complications. With adequate repair, the LVOT is widened, the SAM, MR and outflow gradient are greatly improved. Color flow Doppler of the LVOT should reveal laminar flow. [44] Outflow tract gradient and MR are assessed only after the postcardiopulmonary bypass (CPB) hemodynamics has been optimized. Two important causes of persisting LV outflow gradient are missing a concomitant mid-cavity obstruction and failure to correct mitral valve/papillary muscle abnormalities. [40] Detection of mid-cavity HCM should be carefully assessed especially in the ME views. It may be associated with an akinetic chamber in the apex. Akinetic chamber results in a paradoxical color flow Doppler. Blood is trapped within the apex during systole due to the mid-cavity HCM and flows into the body of the LV during early diastole. [44] Residual gradient also should prompt for careful assessment of abnormalities of the papillary muscle and mitral valve that shift the mitral apparatus and coaptation point anteriorly. Residual MR jets must be assessed qualitatively and quantitatively. Any regurgitant jet that is more than trivial should be studied for direction, size, systolic duration, location and mechanism. Early systolic jets or closing jets are due to irregularities along the coaptation surface and are considered benign, whereas pan-systolic jets represent unaddressed structural defects. [45] The zone of coaptation of the mitral valve leaflets must be studied in the DTGLAX view. A coaptation zone of at least 5 mm is required for adequate mitral valve closure. [45] Another area of concern is excluding ventricular septal defect. Ventricular septal defect can occur in the immediate postoperative period or can occur within days or months after myectomy. It follows excessive septal resection, especially when the septal thickness is <20 mm. [46],[47],[48],[49] Delayed post myectomy ventricular septal defect can occur as early as the third postoperative day. The delayed ventricular septal defect is a postinfarct lesion due to injury to septal perforators during resection, and its location need not be at the site of myectomy. The septum should be carefully examined for any defect in the ME views. Color flow jets flowing across interventricular septum should be differentiated from a coronary-cameral fistula that arises from the transection of the septal perforators. Septal perforators that jet into the LV is considered benign and does not require further intervention. [48] They are identified by their flow only in diastole and from the septum as opposed to septal defect where the flow occurs predominantly during systole and across the interventricular septum. The aortic valve should also be assessed for integrity after HCM correction. [49] Small amount of residual SAM seen by 2D imaging may be accepted in view of the fact that they resolve usually within 2 weeks. [50]

Three-dimensional transesophageal echocardiography

2D TEE images represent only thin slices of the heart, whereas three-dimensional (3D) TEE by spatial reconstruction of TEE images is able to provide a more comprehensive assessment. The three-dimensional geometry of the LVOT can be comprehensively assessed for the location and severity of obstruction and can accurately guide myectomy. [51] Real-time 3D TEE shows excellent correlation with cardiac MRI for measurement of LV wall thickness, volume, and mass and ejection fraction and was found superior to 2D TEE. [52] Three-dimensional TEE is especially helpful in assessing the contribution of SAM and intrinsic mitral valve pathology in the genesis of LVOTO. The measurement of mitral annular diameter, leaflet lengths, excessive length of PML, and the contribution of abnormal bands can be made out by 3D TEE. [53],[54] The en-face view of the mitral valve in 3D aligned to the "surgeon's view" is helpful in identifying the prolapsed mitral scallop and demonstrating the complex anatomy of the mitral valve apparatus. [53] Post repair 3D TEE is helpful in assessing the adequacy of mitral valve repair and relief of LVOTO. [51]

   Surgical procedures Top

Septal myectomy (Morrow's procedure) [3]

The resection is begun by making two parallel longitudinal incisions in the septum, the first beneath the nadir of the right coronary cusp and the second beneath the commissure between the right and the left coronary cusps. These incisions are connected superiorly with a third incision 1.0 cm below the aortic valve, and a deep wedge of septal tissue is resected. Care is taken to carry the incision apically beyond the point of mitral-septal contact.

Extended septal myectomy

Messmer et al. [55],[56] refined the Morrow's procedure by extending the resection more apically to the base of the papillary muscle and by addressing the sub-valvar abnormalities of the mitral valve. The classical resection of Morrow's is extended leftward toward the mitral valve annulus and apically to the bases of the papillary muscles [Figure 3]. All areas of papillary muscle fusion to the septum or ventricular free wall are divided, of the mitral leaflets to the ventricular septum or free wall are divided or excised. [57]

Resection, plication, release

Although extended myectomy relieves LVOTO in most patients, it does not address the problem of abnormally long mitral valve leaflets seen in some patients. The resection, plication, release procedure was devised to address all the phenotypic expressions of HCM and includes extended myectomy (resection), horizontal plication of AML to reduce its anteroposterior length (Plication) and division of any abnormal attachments of the papillary muscles to ventricular wall or AML (release). [58],[59]

Mitral valve replacement

Replacement with low-profile mitral valve prosthesis also reduces the LV outflow gradient and improves symptoms. The major disadvantages of this procedure are the problems of durability, infection, thromboembolism, and anticoagulation associated with prosthetic valves. "Mitral valve replacement is now reserved for significant MR in patients with primary mitral valve disease unsuitable for valve repair". [9],[57]

Early and long-term results

The early reports of surgical myectomy showed mortality ranging from 5% to 10%, [60] the present mortality rates are consistently reported below 2% and approaches close to 0% from several large series making it a safe cardiac surgical procedure. [60],[61],[62],[63] Myectomy provides a long-term survival benefit similar to that of the general population. Postoperative cardiovascular survival rates reported were 98%, 96%, and 87% at 1, 5, and 10 years, respectively. Survival free from HCM-related mortality (heart failure and sudden death) is 99%, 98%, and 95%, respectively. [63] The variables associated with adverse long-term events include older age at surgery (>50 years), female gender, concomitant coronary artery bypass grafting, preoperative atrial fibrillation, and transverse left atrial dimension of >46 mm. [61] Immediate perioperative complications reported include new onset of atrial fibrillation, ventricular septal defect and aortic insufficiency.

   Summary Top

Hypertrophic cardiomyopathy poses many unique challenges regarding the conduct of anesthesia and surgery. Adequate preload, control of sympathetic stimulation and heart rate and increased afterload are required to decrease the LVOTO. The team taking care of HCM patients should be aware of the pathophysiology of this disease [5] as well as it's anesthetic and surgical considerations. TEE is useful in determining the extent of the required resection, evaluating structural abnormalities of the mitral valve, evaluation of residual postmyectomy obstruction, and assessment of post-pump run MR. [6]

   References Top

1.Cleland WP. The surgical management of obstructive cardiomyopathy. J Cardiovasc Surg (Torino) 1963;4:489-91.  Back to cited text no. 1
2.Morrow AG, Reitz BA, Epstein SE, Henry WL, Conkle DM, Itscoitz SB, et al. Operative treatment in hypertrophic subaortic stenosis. Techniques, and the results of pre and postoperative assessments in 83 patients. Circulation 1975;52:88-102.  Back to cited text no. 2
3.Morrow AG. Hypertrophic subaortic stenosis. Operative methods utilized to relieve left ventricular outflow obstruction. J Thorac Cardiovasc Surg 1978;76:423-30.  Back to cited text no. 3
4.Mohr FW, Seeburger J, Misfeld M. Keynote Lecture-Transmitral hypertrophic obstructive cardiomyopathy (HOCM) repair. Ann Cardiothorac Surg 2013;2:729-32.  Back to cited text no. 4
5.Varma PK, Neema PK. Hypertrophic cardiomyopathy: Part 1-Introduction, pathology and pathophysiology. Ann Card Anaesth 2014;17:118-24.  Back to cited text no. 5
[PUBMED]  Medknow Journal  
6.Gajewski M, Hillel Z. Anesthesia management of patients with hypertrophic obstructive cardiomyopathy. Prog Cardiovasc Dis 2012;54:503-11.  Back to cited text no. 6
7.Maron BJ. Hypertrophic cardiomyopathy: A systematic review. JAMA 2002 13;287:1308-20.  Back to cited text no. 7
8.Stevenson LW, Loscalzo J. Cardiomyopathy and myocarditis. In: Longo DL, Fauci AS, Kaslper DL, Hauser SL, Jameson LR, Loscalzo J (editors). Harrison′s Principles of Internal Medicine. 18 th ed. New York: McGraw Hill Medical; 2012. p. 3970-91.  Back to cited text no. 8
9.Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, et al. 2011 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:e783-831.  Back to cited text no. 9
10.Nagueh SF, Bierig SM, Budoff MJ, Desai M, Dilsizian V, Eidem B, et al. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with hypertrophic cardiomyopathy: Endorsed by the American Society of Nuclear Cardiology, Society for Cardiovascular Magnetic Resonance, and Society of Cardiovascular Computed Tomography. J Am Soc Echocardiogr 2011;24:473-98.  Back to cited text no. 10
11.DiNardo JA, Zvara DA, editors. Anesthesia for Cardiac Surgery. 3 rd ed. Massachusetts: Blackwell Publishing; 2008. p. 51-4.  Back to cited text no. 11
12.Gallagher JD. Perianesthetic management of hypertrophic cardiomyopathy. Anesthesiology 2006;105:631.  Back to cited text no. 12
13.Poliac LC, Barron ME, Maron BJ. Hypertrophic cardiomyopathy. Anesthesiology 2006;104:183-92.  Back to cited text no. 13
14.Jain A, Jain K, Bhagat H, Mangal K, Batra Y. Anesthetic management of a patient with hypertrophic obstructive cardiomyopathy with dual-chamber pacemaker undergoing transurethral resection of the prostate. Ann Card Anaesth 2010;13:246-8.  Back to cited text no. 14
[PUBMED]  Medknow Journal  
15.Oliver WC Jr, Mauermann WJ, Nuttall GA. Uncommon cardiac diseases. In: Kaplan JA, Reich DL, Savino JS, editors. Kaplan′s Cardiac Anesthesia. 6 th ed. Missouri: Elsevier; 2011. p. 686-92.  Back to cited text no. 15
16.Sahoo RK, Dash SK, Raut PS, Badole UR, Upasani CB. Perioperative anesthetic management of patients with hypertrophic cardiomyopathy for noncardiac surgery: A case series. Ann Card Anaesth 2010;13:253-6.  Back to cited text no. 16
[PUBMED]  Medknow Journal  
17.Bloor BC, Ward DS, Belleville JP, Maze M. Effects of intravenous dexmedetomidine in humans. II. Hemodynamic changes. Anesthesiology 1992;77:1134-42.  Back to cited text no. 17
18.Kowey PR, Marinchak RA, Rials SJ, Filart RA. Intravenous amiodarone. J Am Coll Cardiol 1997;29:1190-8.  Back to cited text no. 18
19.Stergiopoulos K, Shiang E, Bench T. Pregnancy in patients with pre-existing cardiomyopathies. J Am Coll Cardiol 2011;58:337-50.  Back to cited text no. 19
20.Autore C, Conte MR, Piccininno M, Bernabò P, Bonfiglio G, Bruzzi P, et al. Risk associated with pregnancy in hypertrophic cardiomyopathy. J Am Coll Cardiol 2002;40:1864-9.  Back to cited text no. 20
21.Thaman R, Varnava A, Hamid MS, Firoozi S, Sachdev B, Condon M, et al. Pregnancy related complications in women with hypertrophic cardiomyopathy. Heart 2003;89:752-6.  Back to cited text no. 21
22.Autore C, Brauneis S, Apponi F, Commisso C, Pinto G, Fedele F. Epidural anesthesia for cesarean section in patients with hypertrophic cardiomyopathy: A report of three cases. Anesthesiology 1999;90:1205-7.  Back to cited text no. 22
23.Oakley GD, McGarry K, Limb DG, Oakley CM. Management of pregnancy in patients with hypertrophic cardiomyopathy. Br Med J 1979;1:1749-50.  Back to cited text no. 23
24.Ishiyama T, Oguchi T, Iijima T, Matsukawa T, Kashimoto S, Kumazawa T. Combined spinal and epidural anesthesia for cesarean section in a patient with hypertrophic obstructive cardiomyopathy. Anesth Analg 2003;96:629-30.  Back to cited text no. 24
25.Minnich ME, Quirk JG, Clark RB. Epidural anesthesia for vaginal delivery in a patient with idiopathic hypertrophic subaortic stenosis. Anesthesiology 1987;67:590-2.  Back to cited text no. 25
26.Sharma KC, Brandstetter RD, Brensilver JM, Jung LD. Cardiopulmonary physiology and pathophysiology as a consequence of laparoscopic surgery. Chest 1996;110:810-5.  Back to cited text no. 26
27.Ashidagawa M, Ohara M, Koide Y. An intraoperative diagnosis of dynamic left ventricular outflow tract obstruction using transesophageal echocardiography leads to the treatment with intravenous disopyramide. Anesth Analg 2002;94:310-2.  Back to cited text no. 27
28.Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. Recommendations for chamber quantification: A report from the American Society of Echocardiography′s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005;18:1440-63.  Back to cited text no. 28
29.Williams LK, Frenneaux MP, Steeds RP. Echocardiography in hypertrophic cardiomyopathy diagnosis, prognosis, and role in management. Eur J Echocardiogr 2009;10:iii9-14.  Back to cited text no. 29
30.Cardim N, Perrot A, Ferreira T, Pereira A, Osterziel KJ, Reis RP, et al. Usefulness of Doppler myocardial imaging for identification of mutation carriers of familial hypertrophic cardiomyopathy. Am J Cardiol 2002;90:128-32.  Back to cited text no. 30
31.Bayrak F, Kahveci G, Mutlu B, Sonmez K, Degertekin M. Tissue Doppler imaging to predict clinical course of patients with hypertrophic cardiomyopathy. Eur J Echocardiogr 2008;9:278-83.  Back to cited text no. 31
32.Kato TS, Noda A, Izawa H, Yamada A, Obata K, Nagata K, et al. Discrimination of nonobstructive hypertrophic cardiomyopathy from hypertensive left ventricular hypertrophy on the basis of strain rate imaging by tissue Doppler ultrasonography. Circulation 2004;110:3808-14.  Back to cited text no. 32
33.Sherrid MV, Arabadjian M. Echocardiography to individualize treatment for hypertrophic cardiomyopathy. Prog Cardiovasc Dis 2012;54:461-76.  Back to cited text no. 33
34.Rehfeldt KH, Mauermann WJ, Nuttall GA, Oliver WC Jr. Cardiomyopathies. In: Perioperative Transesophageal Echocardiography. A Companion to Kaplan′s Cardiac Anesthesia. Philadelphia: Saunders; 2013. p. 171-9.  Back to cited text no. 34
35.Sherrid MV, Gunsburg DZ, Pearle G. Mid-systolic drop in left ventricular ejection velocity in obstructive hypertrophic cardiomyopathy: The lobster claw abnormality. J Am Soc Echocardiogr 1997;10:707-12.  Back to cited text no. 35
36.Sherrid MV, Wever-Pinzon O, Shah A, Chaudhry FA. Reflections of inflections in hypertrophic cardiomyopathy. J Am Coll Cardiol 2009;54:212-9.  Back to cited text no. 36
37.Aurigemma G, Battista S, Orsinelli D, Sweeney A, Pape L, Cuénoud H. Abnormal left ventricular intracavitary flow acceleration in patients undergoing aortic valve replacement for aortic stenosis. A marker for high postoperative morbidity and mortality. Circulation 1992;86:926-36.  Back to cited text no. 37
38.Cavalcante JL, Barboza JS, Lever HM. Diversity of mitral valve abnormalities in obstructive hypertrophic cardiomyopathy. Prog Cardiovasc Dis 2012;54:517-22.  Back to cited text no. 38
39.Maron BJ, Harding AM, Spirito P, Roberts WC, Waller BF. Systolic anterior motion of the posterior mitral leaflet: A previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy. Circulation 1983;68:282-93.  Back to cited text no. 39
40.Swistel DG, Balaram SK. Surgical myectomy for hypertrophic cardiomyopathy in the 21 st century, the evolution of the "RPR" repair: Resection, plication, and release. Prog Cardiovasc Dis 2012;54:498-502.  Back to cited text no. 40
41.Yu EH, Omran AS, Wigle ED, Williams WG, Siu SC, Rakowski H. Mitral regurgitation in hypertrophic obstructive cardiomyopathy: Relationship to obstruction and relief with myectomy. J Am Coll Cardiol 2000;36:2219-25.  Back to cited text no. 41
42.Nagueh SF, Lakkis NM, Middleton KJ, Spencer WH 3 rd , Zoghbi WA, Quiñones MA. Doppler estimation of left ventricular filling pressures in patients with hypertrophic cardiomyopathy. Circulation 1999;99:254-61.  Back to cited text no. 42
43.Geske JB, Sorajja P, Nishimura RA, Ommen SR. The relationship of left atrial volume and left atrial pressure in patients with hypertrophic cardiomyopathy: An echocardiographic and cardiac catheterization study. J Am Soc Echocardiogr 2009;22:961-6.  Back to cited text no. 43
44.Nakamura T, Matsubara K, Furukawa K, Azuma A, Sugihara H, Katsume H, et al. Diastolic paradoxic jet flow in patients with hypertrophic cardiomyopathy: Evidence of concealed apical asynergy with cavity obliteration. J Am Coll Cardiol 1992;19:516-24.  Back to cited text no. 44
45.Fischer GW, Anyanwu AC, Adams DH. Intraoperative classification of mitral valve dysfunction: The role of the anesthesiologist in mitral valve reconstruction. J Cardiothorac Vasc Anesth 2009;23:531-43.  Back to cited text no. 45
46.Bartels K, Daneshmand MA, Mathew JP, Glower DD, Swaminathan M, Nicoara A. Delayed postmyectomy ventricular septal defect. J Cardiothorac Vasc Anesth 2013;27:381-4.  Back to cited text no. 46
47.Siegman IL, Maron BJ, Permut LC, McIntosh CL, Clark RE. Results of operation for coexistent obstructive hypertrophic cardiomyopathy and coronary artery disease. J Am Coll Cardiol 1989;13:1527-33.  Back to cited text no. 47
48.Awasthi A, Wormer D, Heggunje PS, Obeid A. Long-term follow-up of acquired coronary artery fistula after septal myectomy for hypertrophic cardiomyopathy. J Am Soc Echocardiogr 2002;15:1104-7.  Back to cited text no. 48
49.Swaminathan M, Debruijn NP, Glower DD, Mathew JP. Unexpected transesophageal echocardiographic finding after septal myectomy. J Cardiothorac Vasc Anesth 2002;16:384-5.  Back to cited text no. 49
50.Ommen SR, Park SH, Click RL, Freeman WK, Schaff HV, Tajik AJ. Impact of intraoperative transesophageal echocardiography in the surgical management of hypertrophic cardiomyopathy. Am J Cardiol 2002;90:1022-4.  Back to cited text no. 50
51.Sadat K, Diddi HP, Klas B, Asaad AH, Çekirdekçi EI, Sungur A, et al. Live/real time three-dimensional transesophageal echocardiographic assessment of ventricular septal volume and mass before and after myectomy in hypertrophic cardiomyopathy. Echocardiography 2013;30:1227-31.  Back to cited text no. 51
52.Bicudo LS, Tsutsui JM, Shiozaki A, Rochitte CE, Arteaga E, Mady C, et al. Value of real time three-dimensional echocardiography in patients with hypertrophic cardiomyopathy: Comparison with two-dimensional echocardiography and magnetic resonance imaging. Echocardiography 2008;25:717-26.  Back to cited text no. 52
53.Jungwirth B, Adams DB, Mathew JP, Swaminathan M, Glower DD, Mackensen GB. Mitral valve prolapse and systolic anterior motion illustrated by real time three-dimensional transesophageal echocardiography. Anesth Analg 2008;107:1822-4.  Back to cited text no. 53
54.Willert JL, Shook D, D′Ambra MN. 3D transesophageal echocardiography: Systolic anterior motion with hypertrophic obstructive cardiomyopathy. Anesth Analg 2006;102:1361-2.  Back to cited text no. 54
55.Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg 1994;58:575-7.  Back to cited text no. 55
56.Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. Circulation 1995;92 9 Suppl: II122-7.  Back to cited text no. 56
57.Minakata K, Dearani JA, Nishimura RA, Maron BJ, Danielson GK. Extended septal myectomy for hypertrophic obstructive cardiomyopathy with anomalous mitral papillary muscles or chordae. J Thorac Cardiovasc Surg 2004;127:481-9.  Back to cited text no. 57
58.Balaram SK, Sherrid MV, Derose JJ Jr, Hillel Z, Winson G, Swistel DG. Beyond extended myectomy for hypertrophic cardiomyopathy: The resection-plication-release (RPR) repair. Ann Thorac Surg 2005;80:217-23.  Back to cited text no. 58
59.Sherrid MV, Chaudhry FA, Swistel DG. Obstructive hypertrophic cardiomyopathy: Echocardiography, pathophysiology, and the continuing evolution of surgery for obstruction. Ann Thorac Surg 2003;75:620-32.  Back to cited text no. 59
60.Maron BJ, Merrill WH, Freier PA, Kent KM, Epstein SE, Morrow AG. Long-term clinical course and symptomatic status of patients after operation for hypertrophic subaortic stenosis. Circulation 1978;57:1205-13.  Back to cited text no. 60
61.Woo A, Williams WG, Choi R, Wigle ED, Rozenblyum E, Fedwick K, et al. Clinical and echocardiographic determinants of long-term survival after surgical myectomy in obstructive hypertrophic cardiomyopathy. Circulation 2005;111:2033-41.  Back to cited text no. 61
62.ten Berg JM, Suttorp MJ, Knaepen PJ, Ernst SM, Vermeulen FE, Jaarsma W. Hypertrophic obstructive cardiomyopathy. Initial results and long-term follow-up after Morrow septal myectomy. Circulation 1994;90:1781-5.  Back to cited text no. 62
63.Maron BJ. Surgical myectomy remains the primary treatment option for severely symptomatic patients with obstructive hypertrophic cardiomyopathy. Circulation 2007;116:196-206.  Back to cited text no. 63

Correspondence Address:
Praveen Kerala Varma
Department of Cardiac Surgery, Division of Cardiac Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum - 695 011, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.135852

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]

  [Table 1], [Table 2]

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