Heart Attack Survivor - a field guide

A secundum atrial septal defect ASD2 is a defect within the fossa ovalis due to deficiency of septum primum Figure 2. It is called a secundum ASD because it represents persistence of ostium secundum or the second opening between the developing atria. There are two mechanisms for an ASD2: Occasionally there can be multiple small holes in septum primum called a cribriform fossa ovalis Figure 3. The interatrial communication is due to failure of obliteration of ostium primum or the first hole between the atria Figure 4.

The resulting deficiency of the central part of the heart includes the inferior basal ventricular septum as well as the AV canal portion of the atrial septum. The inflow ventricular septum is shortened by the deficiency of basal muscular septum. The two principal AV cushions fail to fuse normally resulting in a cleft or zone of apposition between the superior and inferior components of the anterior mitral leaflet Figure 5. The common inlet to the AV orifice is not divided because septum primum does not fuse with the AV cushions.

The AV junction does not indent anteriorly because the inlet does not divide into two separate orifices. Consequently, the aorta does not become wedged between the AV valves.

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The AV node and penetrating bundle are more posterior than usual, lying on the crest of the muscular septum and beneath the inferior tricuspid leaflet. The mechanism is usually tethering of the superior component of the anterior mitral leaflet to the anterior muscular septum by short chordae.

This prevents posterior motion of the leaflet out of the outflow during systole. A fibromuscular ridge or membrane contributes in some cases [ 6 ]. A sinus venosus defect SVD is not actually within the atrial septum Figure 6. Rather, a superior vena cava SVC type of SVD is superior and rightward of the fossa ovalis, between the right cavo-atrial junction and the right upper pulmonary vein s. The mechanism of development is unclear because these structures do not share a common wall early in development.

It seems likely that SVD develop from disruption of the wall between the pulmonary veins and the SVC later in development. The SVD is always associated with anomalous drainage of one or more right pulmonary veins to the cavo-atrial junction. In some cases additional pulmonary veins connect anomalously to the SVC above the cavo-atrial junction. A rare type of SVD, the inferior or right atrial type, has been reviewed recently [ 7 ] and will not be discussed here.

The size of the communication is variable, with complete unroofing of the CS in some cases. The mechanism for development of this defect is unclear because the left cardinal vein and left horn of sinus venosus do not share a common wall with the LA until later in development, suggesting that this defect also results from late disruption of the wall.

Flow across an interatrial communication is determined in part by the size of the defect and in part by the relative ventricular compliances [ 4 ]. Small defects usually less than mm can be restrictive and limit both blood flow and pressure transmission. Flow across a large, unrestrictive defect is dependent on the difference in compliance between the right ventricle RV and LV rather than the pressure difference between the atria.

Since the RV compliance is usually higher than LV, shunt flow is from left to right across the defect. The shunt causes volume loading of the RA and RV, resulting in chamber enlargement [ 8 ]. Increased pulmonary blood flow over time can damage the pulmonary vascular endothelium leading to an increase in pulmonary vascular resistance called pulmonary vascular obstructive disease.

Comorbid conditions in adults such as ischemic and hypertensive heart disease might exacerbate the atrial left-toright shunt by increasing LV end-diastolic pressure and decreasing compliance. Subaortic stenosis can add LV pressure overload to the hemodynamic burden, with secondary LV hypertrophy and decreased compliance.

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Although this does not generally cause perceptible cyanosis, it does create a risk for stroke and brain abscess. Most interatrial communications do not cause symptoms in childhood allowing some to go undetected until adulthood [ 9 ]. Adults typically present with dyspnea, fatigue, palpitations, or atypical chest pain [ 10 ].

Alternatively, an atrial shunt might be discovered fortuitously, for example by echocardiography during evaluation for an arrhythmia. The physical exam is characterized by a widely split and fixed second heart sound S2 due to prolonged RV ejection which delays pulmonary valve closure. Flow across the atrial defect results in maximal filling of the RV during all phases of the respiratory cycle preventing the normal respiratory variation in the duration of RV ejection [ 8 ].

The RV apex is hyperdynamic and a pulmonary ejection murmur is usually audible due to increased RV stroke volume. If the shunt is large, a mid-diastolic tricuspid flow murmur is present as well. A holosystolic murmur at the apex indicates MR and a systolic outflow murmur at the right upper sternal edge subaortic stenosis [ 6 ]. The chest radiograph often shows an enlarged RA, RV and pulmonary trunk. Echocardiography is the primary diagnostic tool for interatrial communications Figures 7, 8 and 9 [ 11 ]. Transesophageal echo is indicated in adults if the transthoracic exam is inadequate.

Cardiac magnetic resonance imaging CMR is probably the modality of choice for SVD Figure 10 because of its ability to detect anomalously connecting pulmonary veins [ 12 ]. Catheterization is rarely indicated for diagnosis of an interatrial communication [ 4 ]. Closure of an interatrial communication is indicated even for asymptomatic patients if the right heart is enlarged [ 13 ]. Closure of an ASD2 can be accomplished by surgery or interventional catheterization Figure 11 [ 14 ]. ASD1, on the other hand, is a surgical defect.

Congenital Heart Defects in Adults : A Field Guide for Cardiologists

Repair involves patch closure of the defect and closure of the cleft or zone of apposition in the mitral valve. Failure to close the cleft in the anterior mitral leaflet often results in progressive MR and additional surgery [ 17 ]. Various techniques have been adapted to treat LV outflow obstruction, ranging from resection of fibrous tissue and removal of abnormal chordal attachments to a modified Konno procedure [ 18 , 19 ]. The SVD is a surgical defect as well. In most cases of SVD, the opening between the right pulmonary veins and the cavo-atrial junction can be closed using a patch, with the pulmonary veins draining to the LA behind the patch and the SVC to the RA in front of the patch Figure 6.

If there are additional pulmonary veins connecting to the SVC more superiorly, a different approach is indicated. The SVC is transected and over sewn proximally just above the superior-most pulmonary vein. The mouth of the SVC and any veins draining to the cavo-atrial junction are baffled through the defect to the LA. This approach is less likely to cause sinus node dysfunction [ 20 , 21 ]. The CSD can often be closed with a patch or by direct suture.

Allowing cardiac veins to drain to the LA has little effect on systemic oxygen saturation. Atrial arrhythmias are the most frequent late complication. Patients repaired early in life have a small risk for supraventricular tachycardia and the risk increases with advancing age at repair.

If repair is undertaken in adults greater than 40 years of age, pre-operative or early post-operative atrial flutter or fibrillation is an independent predictor of late recurrence of these rhythms [ 22 ]. The occurrence of atrial arrhythmias does not appear related to surgical technique [ 23 ], except in SVD where the two-patch technique is associated with a greater risk of sinus node dysfunction compared with transection of the SVC [ 15 , 16 ]. Atrial fibrillation appears to have an earlier age of onset less than 30 years in patients with ASD1 than in other atrial shunts, likely due to concomitant left AV valve regurgitation.

In addition, atrial arrhythmias are a common cause of deterioration [ 24 - 27 ]. Late acquired heart block can be seen in ASD1, even in unrepaired patients [ 24 ]. Current guidelines recommend periodic Holter monitoring to detect AV conduction defects [ 13 , 27 ].

Pulmonary hypertension, another important late complication, is rare in patients operated before 25 years of age, and the risk increases with advancing age at repair [ 1 , 11 , 12 ]. While related, in part, to increased pulmonary blood flow, the exact mechanism is unknown. Mitral regurgitation and LV outflow obstruction are other important late complications in ASD1 [ 13 , 26 ]. Patients who undergo repair of an atrial communication prior to 25 years of age appear to have a normal lifespan and low risk for pulmonary hypertension and arrhythmias [ 28 ].

Closure after 25 years but prior to 40 years increases the risk of atrial arrhythmias [ 22 ]. Repair after age 40 years reduces cardiovascular complications Figure 12 but does not clearly provide a mortality benefit [ 15 ]. Outcomes for repair of ASD1 in adulthood are quite good with low operative risk [ 25 - 29 ].

The primary abnormality in Ebstein anomaly is apical displacement of the functional annulus of the TV due to failure of delamination of the septal and sometimes posterior leaflets during embryological development Figure In addition, the axis of the TV is rotated from a base-apex direction to a diaphragmatic wall-outflow direction. The anterior leaflet is sometimes redundant and often has fenestrations. The leaflets are tethered to the underlying myocardium by short chordae.

Papillary muscles can be attached directly to the leaflets by muscular bands [ 33 , 34 ]. The result most often is tricuspid regurgitation TR with a large, central regurgitant orifice [ 6 ], but in some cases tricuspid stenosis is predominant Figure 14 [ 33 ]. Associated lesions include an interatrial communication, and less commonly muscular ventricular septal defect VSD or patent ductus arteriosus.

In more complex forms of Ebstein anomaly, pulmonary stenosis or atresia or left-sided abnormalities such as mitral stenosis or regurgitation can be seen [ 35 ]. The conduction system is often abnormal, with prolonged conduction in the enlarged RA. There is also prolonged infranodal conduction due to lengthening or stretching of the conduction system within the atrialized RV [ 36 ].

TR reduces the forward stroke volume of the already hypoplastic functional RV. The atrialized RV balloons out during atrial systole, acting as a passive reservoir rather than participating in coordinated atrial contraction, thus impeding atriosystolic filling of the RV [ 38 ]. The small functional RV is often less compliant than the LV, favoring right-to-left atrial shunting. In patients with predominantly tricuspid stenosis, the valve directly limits forward flow and favors interatrial shunting. The pulmonary valve PV and pulmonary arteries are often smaller than normal, increasing impedance to forward flow and favoring TR.

Over time, there is RV dilation and thinning of the free wall, both from TR [ 33 ] and possibly from an inherent myopathy [ 38 ]. With severe RV enlargement, the ventricular septum shifts leftward adversely affecting LV filling [ 33 ]. This adverse ventricular-ventricular interaction can reduce cardiac output, especially with exercise. The severity of disease dictates when and how patients present. The most severe forms of Ebstein anomaly present with cyanosis and heart failure in the neonatal period while adults might present with only an arrhythmia associated with an accessory pathway [ 6 ].

Adult Ebstein patients also exhibit cyanosis, exercise intolerance, dyspnea, fatigue, or right-sided heart failure [ 39 ]. The cardiac exam is often described as a musical cacophony. The first heart sound is widely split, with a loud tricuspid component due to increased excursion of the anterior tricuspid leaflet and delayed closure of the abnormal TV [ 6 , 40 ]. There are often ventricular filling sounds third or fourth heart sound due to abnormal ventricular compliance.

The sum of all this is a complex quadruple rhythm. A holosystolic murmur heard best at the lower left sternal border is due to TR. Hepatomegaly from hepatic congestion usually indicates right heart failure [ 6 ]. The QRS is wide with a right bundle branch block pattern due to infra- Hisian conduction disturbances [ 35 ].

The chest radiograph typically shows cardiac enlargement with a globular contour [ 6 , 35 ]. Echocardiography is diagnostic Figure 15 and useful for evaluating anatomy and function of the TV, the size of the functional RV, and presence of associated defects [ 6 , 41 , 42 ]. It is indicated prior to surgical intervention on the valve and is probably the best method for serial evaluation of adult patients.

Pulse oximetry is useful to quantify cyanosis at rest and during exercise [ 13 ]. Exercise testing is an objective method to follow functional capacity. Extended ECG monitoring is useful to detect and diagnose arrhythmias [ 13 ]. Medical therapy of Ebstein anomaly is limited to management of complications. Patients with refractory atrial fibrillation might benefit from pharmacologic rate control and anticoagulation [ 13 ].

Some arrhythmias are controllable with medication. Diuretic therapy is useful to maintain fluid balance in heart failure. Transcatheter ablation is the standard treatment of an accessory pathway or other arrhythmia substrate but success rates tend to be lower and recurrence rates higher than in the structurally normal heart [ 44 ]. Percutaneous closure of an ASD2 might be useful in select patients with Ebstein anomaly, although there are few supporting data. Patients with a predominately left-to-right shunt are most likely to benefit.

Cyanotic patients can be harmed by ASD2 closure. If this procedure is undertaken, test occlusion of the defect must be performed to ensure that systemic blood pressure and cardiac output can be maintained [ 45 ]. Prior to surgery, all patients should undergo an invasive electrophysiology study to localize and ablate any accessory pathway s.

If an arrhythmia is present and not amenable to percutaneous treatment, then arrhythmia surgery e. The objectives of surgery are to improve TV function and increase right heart output. The general strategy includes partial or complete closure of any interatrial communication, repair or replacement of the TV, and reduction of RA size. Table 1 summarizes the surgical strategies that have been employed [ 46 - 49 ]. Atrial tachyarrhythmias occur in one-third of post-operative patients [ 50 ]. Half of patients have multiple connections [ 6 ] and the pathways can be located in the atrialized RV with abnormal morphology of the endocardial activation potentials [ 51 ] making ablation difficult.

Identification of patients at risk is challenging [ 6 , 53 - 55 ]. While fetal or neonatal presentation of Ebstein anomaly is associated with a poor outcome [ 39 , 56 ], adults have a much better prognosis [ 52 , 57 ]. Surprisingly, supraventricular arrhythmia does not appear to be associated with worse outcome [ 39 , 57 , 58 ]. There are no randomized trials comparing surgical and non-surgical management of Ebstein anomaly.

Atrial arrhythmia is the most frequent early complication. Survival and functional status did not differ significantly between groups undergoing TV repair or replacement [ 50 , 59 ]. Most patients with CTGA are now diagnosed in infancy or childhood. Some without associated defects go undetected until the 3rd to 6 th decades and rare patients survive a lifetime with no symptoms [ 60 , 61 ]. Consequently, the population followed in most adult congenital heart disease clinics is a mix of operated and unoperated patients.

There are two types of CTGA. In the most common type, the atria and the abdominal organs are in the usual locations situs solitus. Further, the great arteries are transposed so that the left-sided aorta is aligned with the RV and the right-sided pulmonary artery with the LV. Systemic venous blood reaches the pulmonary artery through the LV and pulmonary venous blood the aorta through the RV [ 62 ]. A much less common form of CTGA occurs in situs inversus and is the mirror image of the type described above. In this type, there is inversion or left-right mirror imagery of the atria and abdominal organs.

Here the systemic venous blood returns to the left-sided RA, left-sided LV and left-sided and posterior pulmonary artery. Pulmonary venous blood returns to the right-sided LA, right-sided RV and rightsided and anterior aorta. Often there is also an additional posterior AVN, but it is usually hypoplastic and rarely connects to a penetrating bundle [ 66 ].

This anterior location of the AVN and penetrating bundle makes them vulnerable to complete heart block [ 6 ]. The bundle branches are inverted along with the ventricles. Because of the anterior location of the node and penetrating bundle, the conduction system passes in the superior rim of a VSD [ 66 ].

The coronary anatomy is quite different from the normal heart. The accompanying article by Baraona et al. In the absence of associated defects, the physiology in CTGA is normal. A VSD plus pulmonary stenosis can result in a right-to-left shunt and cyanosis like tetralogy of Fallot or a balanced circulation with only a small shunt in one direction or the other.

Isolated pulmonary stenosis causes pressure overload of the LV and if severe can cause failure of the pulmonary ventricle. The systemic RV fails sooner with associated defects and later without Figure Without associated defects, CTGA patients can be asymptomatic until the third to sixth decades [ 60 , 61 ]. Typical presenting symptoms include a murmur, cyanosis, bradycardia, heart failure, and arrhythmia [ 68 ]. In some cases the diagnosis is made incidentally by cardiac testing for other reasons.

Physical exam reveals a single, loud S2 due to the anterior location of the aorta [ 62 ] and difficulty hearing the soft closure sound of the posterior pulmonary artery [ 68 ]. A holosystolic murmur at the left sternal border, often with a thrill, indicates a VSD [ 69 ]. Pulmonary stenosis causes a systolic ejection murmur at the left or right upper sternal border [ 70 ]. Cyanosis and clubbing could be due to pulmonary stenosis with VSD tetralogy of Fallot physiology or to Eisenmenger syndrome [ 13 ].

A holosystolic murmur at the apex is due to TR [ 13 ]. Q waves in the inferior ECG leads are due to right-to-left septal depolarization and can be misinterpreted as a prior inferior myocardial infarction [ 70 ]. About one-half of patients have 1st degree AV block and the risk of 3rd degree AV block increases with age [ 69 , 70 ]. The P wave is negative in lead I in CTGA in situ sinversus because the atria are inverted; however, ventricular septal activation is normal because the ventricles are normally located [ 62 ].

Signs on the chest radiograph suggestive of CTGA are a prominent left-sided ascending aorta [ 62 ] and dextrocardia [ 70 ]. Two-dimensional echocardiography is diagnostic [ 62 , 71 ]. CMR is the standard for assessment of ventricular size and function, and can be useful to define anatomy if echocardiographic windows are poor Figure 19 [ 13 ]. Extended ECG monitoring is used to diagnose arrhythmias and to estimate average and slowest heart rate in patients with heart block. Exercise testing provides an objective assessment of functional capacity. Cardiac catheterization can be useful to obtain physiological information or if non-invasive testing is not diagnostic [ 13 ].

Medical therapy for CTGA is useful to control arrhythmias [ 13 ] and to treat heart failure. The optimal medical strategies for treatment of systemic RV dysfunction are unknown. Diuretic therapy is effective for management of fluid balance.

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It is unclear if renin-angiotensin activation plays a role in systemic RV dysfunction [ 73 ]. On the other hand, a small pilot study of carvedilol in CTGA patients with RV dysfunction showed positive remodeling and increased exercise duration [ 74 ]. Invasive electrophysiology treatment is indicated for atrial tachyarrhythmias catheter ablation and for bradycardia due to heart block pacemaker therapy.

Single site pacing can induce dyssynchrony and rightward septal shift can worsen TR [ 13 ]. Biventricular pacing in CTGA is difficult due to the unusual cardiac venous anatomy [ 75 ]. In adolescent and adult patients, surgical therapy is usually directed to a specific hemodynamic abnormality. Patients with severe or progressive TR are candidates for TV replacement [ 13 ].

Timing of surgery should avoid deterioration of RV function [ 76 ]. Closure of a VSD should be considered if the RV is dilated and pulmonary vascular resistance is not significantly elevated. Severe aortic regurgitation likely from progressive root dilation with RV dilation should be addressed before RV function deteriorates.

Relief of isolated pulmonary stenosis has been advocated, but it is not clear that this is beneficial unless LV pressure is suprasystemic. Some highly select adult patients with CTGA are candidates for an anatomic correction. The success of anatomic repair is dependent on the LV being adequately prepared to generate systemic blood pressure [ 69 ]. Included are patients with severe, but remediable, pulmonary stenosis and those with a large outlet VSD.

The procedure switches both venous inflow Mustard and arterial outflow arterial switch or Rastelli operation, that is baffling the LV to the aorta through the VSD and placement of a RV to pulmonary artery conduit [ 13 ]. Adult patients with symptomatic RV failure are candidates for heart transplantation because re-training the LV to perform systemic work after years of functioning as the pulmonary ventricle has been mostly unsuccessful [ 78 ].

Previously operated CTGA patients might also undergo surgery for various reasons including replacement of a dysfunctional LV- or RV-to-pulmonary artery conduit and aortic valve surgery for aortic regurgitation [ 13 ]. TR begins in the second decade, becomes moderate or more in the third decade, and increases in severity and prevalence thereafter.

Progressive TR begets more dilation of the systemic RV, which in turn contributes to more regurgitation [ 70 ]. Congestive heart failure with pulmonary edema often ensues between the fourth and sixth decades [ 60 ]. Aortic regurgitation, not previously reported in CTGA, is now known to be a frequent problem in this population [ 69 ]. Outcomes for conventional repair have improved from lessons learned over the past three decades. The outcomes for various cohorts are shown in Table 2 [ 79 - 83 ]. Infants with DTGA present with cyanosis in the first days of life.

Consequently, patients presenting to an ACHD center have had corrective surgery in infancy or childhood. The primary abnormality in DTGA is ventriculo-arterial discordance. The atria and ventricles are normally located but the great arteries are aligned with the incorrect ventricle, that is, the aorta is aligned with the RV and the pulmonary artery with the LV [ 62 ]. The aorta is usually anterior and rightward of the pulmonary artery but the great arteries can be side-by-side and rarely the aorta is posterior or anterior and leftward [ 6 ].

Coronary artery anatomy is variable and important for the arterial switch operation ASO [ 85 ]. The article by Baraona et al. Patients born before the early s most likely underwent an atrial switch operation Mustard [ 86 ] or Senning [ 87 ] or a Rastelli [ 88 ] operation. Patients born after the late s were most likely repaired using the ASO Figure After an atrial switch operation the ventricular and arterial anatomy are unchanged.

A baffle is placed in the atria to redirect systemic venous blood to the MV and pulmonary venous blood to the TV Figures 20, In contrast, after the ASO [ 89 ] the great arteries are inverted so that the aorta connects with the posterior root previously pulmonary root and the pulmonary artery with the anterior root Figures 20, The aorta is pulled through between the branch pulmonary arteries allowing the branches to straddle the aorta.

The coronary arteries are translocated from the anterior to the posterior root Figure A Rastelli operation has been used in patients with a large VSD and severe pulmonary stenosis Figure Here the LV is baffled to the aorta through the VSD, the pulmonary trunk is closed, and a conduit is placed from the RV to the distal pulmonary artery [ 88 ].

There are alternative operations that accomplish the same type of repair and might have advantages in specific cases [ 90 ]. Prior to corrective surgery, the systemic and pulmonary circulations are in parallel instead of in series. Consequently, desaturated blood from the systemic veins is returned to the body and saturated blood from the pulmonary veins is returned to the lungs.

At repair, the circulations are placed in series either by switching the inflow sources atrial switch operation or by switching the outflows arterial switch operation and Rastelli. In addition to routine care, patients after atrial switch operation might present with fatigue, arrhythmia, venous congestion, or symptoms of heart failure. Patients are also referred during pregnancy for more intensive surveillance. Subpulmonary stenosis, a frequent finding, is indicated by an ejection murmur higher up the left sternal border.

Venous congestion or hepatomegaly could signal systemic venous pathway obstruction or heart failure.

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Patients who have had an ASO are usually asymptomatic but might complain of chest pain or exercise limitation. The physical exam is usually unremarkable but a pulmonary outflow murmur or a diastolic murmur of pulmonary or aortic insufficiency might be audible. Various rhythm abnormalities might be evident including bradycardia, junctional rhythm, or complete heart block [ 13 ].

The chest radiograph often shows cardiac enlargement. The echocardiogram might not demonstrate the atrial baffle and venous pathways adequately after an atrial switch operation. CMR is excellent for anatomic evaluation, measurement of ventricular size and function and myocardial characterization Figures 24, CT angiography can be used for functional assessment in patients with an implantable device such as a permanent pacemaker or automated defibrillator and is excellent for coronary artery anatomy [ 91 ].

Extended ECG monitoring is useful to detect and diagnose arrhythmias. Exercise testing is an excellent method to follow functional capacity or detect ischemia from coronary artery abnormalities. After an ASO the echocardiogram shows the anterior pulmonary artery paralleling the aorta and the branch pulmonary arteries passing posteriorly on either side of the ascending aorta. CMR demonstrates overall anatomy, coronary artery anatomy, and ventricular size and function Figure CT angiography is also useful for assessment of the coronary arteries. CMR provides anatomic evaluation as well as functional assessment after the Rastelli operation Figures 27, Sinus node dysfunction is the most frequent complication of an atrial switch operation.

Tachy-brady syndrome is common in this setting as is atrial flutter. Atrial tachyarrhythmias during the operative period, permanent heart block, and small size at surgery are independent risk factors for sudden death [ 92 ]. Risk factors are unclear, but excess hypertrophy is likely to be important [ 6 , 95 ].

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Recurrent ischemia contributes to ventricular dysfunction as evidenced by regional wall motion abnormalities, perfusion defects and late gadolinium enhancement documented decades after a Mustard procedure [ 96 ]. TR usually accompanies RV dysfunction and can contribute to further deterioration [ 93 ]. Other late complications include venous pathway obstruction and baffle leaks Figures 24, The SVC pathway is most often involved and usually decompresses via the azygos vein so that adults are rarely symptomatic [ 97 ]. It is usually discovered during placement of a transvenous pacemaker for sinus node dysfunction.

Inferior vena cava pathway obstruction is rare [ 13 ]. Baffle leaks are more frequent but usually small. These persistent communications can be a source of paradoxical embolization especially if a transvenous pacemaker is in place [ 97 ]. Obstruction of the pulmonary venous pathway Figure 25 is more likely with the Senning operation but is rare late after surgery [ 97 ]. Pulmonary venous pathway obstruction is another cause of elevated pulmonary artery pressure [ 98 ]. Complications are mainly conduit obstruction and subaortic stenosis from inadequate enlargement of the VSD [ 99 ].

LV dysfunction has been described mostly in the setting of severe subaortic stenosis. There is a small but persistent incidence of sudden death, presumed to be arrhythmic in nature [ 99 ].

Heart Attack Survivor - A Field Guide

Pulmonary artery stenosis is the most frequent complication following the ASO. Mechanisms include inadequate growth of the suture line, scarring and retraction of the material used to fill the coronary artery button sites, and tension at the anastomotic site if there is inadequate mobilization of the distal pulmonary arteries [ ].

Arrhythmia is infrequent and sudden death is rare [ 6 ]. The LV in the systemic position maintains good function over time. There is a modest risk for neo-aortic valve regurgitation related in part to neo-aortic root dilatation. Patients with a VSD tend to be at higher risk for neo-aortic valve regurgitation [ ]. Although pulmonary hypertension after the ASO is infrequent, it was a cause of late death in one study [ ].

Arrhythmia management is the most common treatment. Medical or transcatheter treatment of atrial tachyarrhythmia can be challenging. Sinus node dysfunction with tachybrady syndrome is an indication for pacemaker therapy. SVC pathway obstruction can be treated by stent placement, but it is important to define the coronary artery anatomy before undertaking an interventional procedure at the base of the heart [ 67 ].

A baffle leak can often be closed percutaneously with a device. Heart failure symptoms are usually treated with an ACE inhibitor and beta blockade but there is little evidence of efficacy []. Diuretic therapy can be used to maintain fluid balance. Heart transplantation should be considered for end-stage heart failure in atrial switch patients. Replacement of the RV-PA conduit or homograft is the most frequent re-operation after the Rastelli operation.

Enlargement of the VSD to alleviate subaortic stenosis is a less frequent secondary procedure. Stent placement is usually effective for branch pulmonary artery stenosis. Dense scarring of the proximal outflow renders it less amenable to percutaneous therapy and usually requires re-operation. The late survival is higher for the ASO compared with the atrial switch procedures, with fewer long-term complications [ ]. TOF results from leftward and superior displacement of the infundibular or outlet septum, apparently related to abnormal rotation of the outflow during embryogenesis.

In extreme cases the RV outflow and even the pulmonary trunk are atretic [ 62 ]. The accompanying article in this issue by Baraona et al. Patients presenting to an ACHD center have undergone repair in infancy or childhood. Patch augmentation of the RV outflow, division or resection of obstructing muscle, and bypass of obstruction using a RV-pulmonary artery conduit are typical approaches to repair.

Until the last decades wide patch augmentation of the outflow was standard treatment to avoid any residual stenosis, at the expense of creation of free pulmonary regurgitation PR Figure More recently, the emphasis has shifted to preservation of PV function as the late deleterious effects of chronic PR have become apparent. Patients repaired in the last 2 decades are likely to have had a transatrialtranspulmonary approach with limited or no infundubulotomy. Efforts are now made to avoid a trans-annular patch [ 62 ] or to place the patch in such a way as to preserve valve function as much as possible.

In patients with pulmonary atresia or with a major coronary artery crossing the RVOT, an RV-to-pulmonary artery conduit is used Figure Additional defects such as ASD2 are closed at the time of complete repair and any previously constructed shunt Figure 31 taken down [ 6 ]. The physiology of TOF depends on the severity of outflow obstruction and can vary from absence of cyanosis pink tetralogy to ductus arteriosus-dependent pulmonary circulation in cases with pulmonary atresia.

After repair the majority of patients have normal oxygen saturation and no residual shunt. The predominant physiology is RV volume overload from moderate or more PR. Few patients have residual pulmonary stenosis. RV dysfunction and failure as a consequence of chronic volume overload are seen late after repair. LV dysfunction is also seen late after repair, even in the absence of a residual VSD or other volume overload [ ].

The mechanism remains unclear. The unoperated adult with TOF is rarely encountered in developed countries but is less rare where access to health care is more limited. Cyanotic and clubbed, these patients present with exercise limitation, secondary erythrocytosis, stroke or heart failure. S2 is usually single and patients with a patent RV outflow have a systolic ejection murmur in the pulmonary area while those with pulmonary atresia have continuous murmurs over the chest and back due to aorto-pulmonary collaterals [ 13 ]. Fortunately, the good news is that your healthcare team is with you every step of the way.

This second chance begins the ongoing journey to heart health and well-being. Frequency of another heart attack in the United States. Risk factors that can affect your chance of another heart attack are your age, your medical history and other health conditions you may have. The risk of a recurrent attack can be greatly reduced by quitting smoking, exercising and following a healthy diet. You are not alone.

You and your healthcare team will work together to come up with the right care plan for you. Most patients have to adjust to life after a heart attack, including starting new medications to lower the chance of another heart attack or dying from one. Speak with your doctor about a possible treatment option for you or your loved one. Register with Survivors Have Heart and learn more about life after a heart attack. By completing this registration, you are confirming that you are at least 18 years old and a United States citizen.

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