Postinfarction Ventricular Septal Rupture

Anterior myocardial infarction is typically associated with apical VSDs whilst inferior myocardial infarctions are more commonly associated with basal VSD or posterior papillary muscle rupture. After confirmation of diagnosis by echocardiography or right heart catheter, which reveals a step up in oxygenation at ventricular level, urgent referral to a surgical centre is required, the outlook without surgical repair being extremely poor.

Anterior myocardial infarction associated with apical VSD carries a better surgical outlook than inferior myocardial infarction associated with basal VSD.

Reference

• Moore CA, Nygard TW, Kaiser DS et al. Postinfarction ventricular septal rupture: the importance of location of infarction and right ventricular function determining survival. Circulation 1986;74:45.

ACE inhibitor-induced angioedema

ACE inhibitor associated angioedema is a well-recognised complication of therapy and may not develop straight away. It is therefore often inappropriately ruled out as a potential cause for the angioedema. It usually resolves rapidly on stopping the ACE inhibitor. 

Management of acute pulmonary oedema

Unless it is definitely known that a patient has a tendency to retain carbon dioxide, all patients with severe breathlessness should be given high flow oxygen via a reservoir bag once it has been established that their airway is clear.

After the patient has been started on high flow oxygen, give frusemide 40-80 mg IV and diamorphine 2.5-5 mg IV. If matters do not improve consider isosorbide dinitrate 2-10 mg/hr IV. If matters worsen, then call the ICU sooner rather than later (assuming that the man’s condition prior to this acute presentation means that this is appropriate).

Concurrently try to establish a cause for the acute deterioration: has he had a myocardial infarction? If so, would he benefit from thrombolysis?

Tetralogy of Fallot

In Tetralogy of Fallot (right ventricular outflow tract obstruction, ventricular septal defect, right ventriuclar hypertrophy, over-riding aorta) the severity of clincial presentation is dependent upon the degree of obstruction to the right ventricular outflow tract. This is often dynamic (muscular bulge below the pulmonary valve) and will ultimately determine the degree of right to left shunting (and hence cyanosis etc.).

The degree of obstruction often progresses after birth and therefore children may present at a later date (although usually within the first two years).

Heart Failure and Cardiac Transplant

Patients with heart failure are considered for cardiac transplantation when significant symptoms persist despite maximal medical therapy. Due to the shortage of donors clinical guidelines have been established highlighting patients most suitable for transplantation. Significant impairment of renal function is generally considered to be a contraindication, assuming this is not reversible. Patients with prior history of cancer may be considered if there is no evidence recurrence (> 5 years on from diagnosis of cancer).

Cholesterol-Lowering Therapy in Patients With Coronary Heart Disease

Drug treatment to lower serum cholesterol should be based on a person’s risk of an ischaemic heart disease (IHD) event rather than initial cholesterol level. Any person who has had a myocardial infarction has about a 10% chance (without treatment) of dying from ischaemic heart disease in the following year and about a 5% chance of IHD death in each year thereafter. All such people (in the absence of contraindications to the specific drugs) qualify for HMG coenzyme A reductase inhibitor therapy (Statins) regardless of their cholesterol level.

There is a constant proportional relationship between serum cholesterol and disease risk, so any reduction in cholesterol level from any starting point leads to the same proportional reduction in IHD risk. Those people with the highest absolute starting risk (namely those with pre-existing IHD, such as this man who has had an AMI) stand to benefit the most.

Non-pharmacological means of serum cholesterol reduction are far less effective, and whilst important are inadequate in this patient.

Reference

• http://circ.ahajournals.org/content/95/6/1683.full

Management of Atrial Fibrillation

In a patient with a probable first episode of AF an attempt should be made to restore sinus rhythm. However, if AF has been present for >48 hrs – as seems very likely in this case – it is necessary to anticoagulate before cardioversion, unless it can be documented by trans-oesophageal echocardiography (TOE) that the left atrium is free of thrombus. If this were the case, then cardioversion within the next 24 hours would be the preferred management option, with warfarinisation for a month afterwards (which is a high risk period for thromboembolism).

Identification and management of patients with failed thrombolysis

The best way to manage patients with failed thrombolysis is with rescue percutaneous transluminal coronary angioplasty (PTCA) in patients still within 12 hours of presentation (REACT and other studies).

Reference

• Oldroyd KG. Identifying failure to achieve complete (TIMI 3) reperfusion following thrombolytic treatment. Heart 2000; 84: 113-115.

Infective Endocarditis in Intravenous Drug Abusers

In intravenous drug abusers Staph aureus accounts for 50% of cases of infective endocarditis, with other causes being enterococci (10%), Strep viridans (5%), gram negative bacteria (5%), other bacteria (5%), fungi (5%) and polymicrobial infection (5%). Coagulase-negative staphylococci account for less than 5%.

By contrast, in patients who do not abuse drugs intravenously (and do not have prosthetic valves) the frequency of infection is as follows: Strep viridans 35%, enterococci 25%, Staph aureus 23%, culture negative 5-10%, other identified organisms 5-10%.

Antihypertensive drugs in pregnancy

Evidence underpinning the choice of anti-hypertensive therapy in pregnancy is inadequate to make firm recommendations. There are no reports of serious effects with methyl-dopa following long and extensive use. Calcium antagonists, labetalol and hydralazine are commonly used, particularly for resistant hypertension in the third trimester. However, angiotensin-converting enzyme (ACE)-inhibitors should be avoided because they may cause oligohydramnios, renal failure and intra-uterine death.


A.
Hydralazine
B.
Labetalol
C.
Lisinopril
D.
Methyl-dopa
E.
Nifedipine.

Your Answer was: C
Correct Answer: C
Comment

Atrial Myxoma

Atrial myxomas are the commonest form of cardiac tumour. They far more commonly arise in the left atrium, most frequently attached to the inter-atrial septum. Systemic embolic complications are common and can be devastating. Hence, unless severe co-morbidity precludes anaesthesis, immediate surgical removal is advocated.
Patients may present with dyspnoea, evidence of systemic embolisation or constitutional upset with fever and elevated inflammatory markers.

Risk factors for hypertrophic cardiomyopathy

Major risk factors for hypertrophic cardiomyopathy are:
▪ Cardiac arrest (ventricular fibrillation)
▪ Spontaneous sustained ventricular tachycardia
▪ Family history of sudden death
▪ Minor risk factors
▪ Unexplained syncope
▪ Left ventricualr wall thickness>30mm
▪ Abnormal blood pressure on exercise(failure to rise from baseline by 25mmHg)
▪ Non sustained Ventricular tachycardia
▪ Left ventricular outflow obstruction
▪ Microvascular obstruction
▪ High risk genetic defect.

Drug induced QT prolongation and torsades de pointes

Fig 1: Torsades de Pointes is a rapid ventricular rhythm caused by low potassium, medications (those that block potassium channels), or congenital abnormalities (e.g. Long QT Syndrome) that lengthen the QT interval. The rate is variable 250 and 350 per minute, in brief episodes.

Drugs that may cause torsade de pointes include:

• Disopyramide
• Dofetilide
• Ibutilde
• Procainamide
• Quinidine
• Sotalol
• Bepridil
• Amiodaone
• Arsenic trioxide
• Cisapride
• Erythromycin
• Doperidone
• Droperidol
• Chlorpromazine
• Haloperidol
• Thioridazine
• Pimozide
• Methadone.

Reference

1. Roden D.M. Drug induced prolongation of the QT interval. N Engl J Med 2004; 350:1013-1022.

Source: Fig 1,

Effect of coronary artery bypass graft surgery on survival

Fig 1: CABG

Coronary artery bypass grafting has been shown to improve survival in patients with left main stem stenosis (> 60%), triple vessel disease and impaired left ventricular function and triple vessel disease with proximal left anterior descending artery disease, when compared to medical therapy.

Fig 2: Left anterior oblique view showing a calcified lesion in the left coronary trunk that encompasses the origin of the  circumflex artery

Angioplasty is exceedingly high risk and therefore is only contemplated when patients are deemed as non-operative candidates.

Reference

1. Yusuf S, Zucker D, Peduzzi P, et al. Effect of coronary artery bypass graft surgery on survival. Overview of 10-year results from randomized trials by the Coronary Artery Bypass Graft Surgery Trialists Collaboration. Lancet 1994; 344: 563-570

Source: Fig 1, Fig 2, 

Congenital Heart Disease and Pregnancy

Pulmonary hypertension of any cause is associated with a 50% maternal mortality. Other high-risk cardiac conditions are severe mitral, pulmonary or aortic stenosis and Marfan's syndrome with a dilated aortic root. Intracardiac shunts without pulmonary hypertension are relatively safe but require closer follow-up. Operated tetralogy of Fallot without residual pulmonary stenosis is lower risk; coarctation is associated with dissection and is intermediate risk.

Features of severe aortic incompetence

Severe aortic incompetence is suggested by the presence of one or more of the following clinical features:
1. Short early diastolic murmur (diastolic pressure in the left ventricle rapidly approaches that in the aorta)
2. Wide pulse-pressure
3. Displaced, hyperdynamic apex beat - implying significant volume overload.

The Austin-Flint murmur may be heard in aortic incompetence (fluttering of the anterior mitral valve leaflet due to turbulance from the regurgitant jet). Whilst a normal heart size on chest radiograph does not preclude a diagnosis of severe aortic incompetence (e.g. acute), it is far more commonly enlarged.

Secundum Atrial Septal Defects

Secundum atrial septal defects are often not identified in childhood and can present with non specific symptoms such as lethargy. The first heart sound is often split but equally may be normal. The definitive investigation is transthoracic echocardiography. This will demonstrate first of all the anatomy and secondly using doppler indicate any significant shunting.

Ostium secundum defects are more midseptal and by far more common than primum defects which are more inferiorly displaced towards the AV valve. Primum defects are often associated with anomalies of the mitral and/or tricuspid valve, and as such patients more commonly present in childhood.

It is clear from the clinical picture that this is not a patent ductus arteriosus. Patent foramen ovale (PFO) is a common condition and generally benign. There may be some left to right flow on doppler imaging but this will not be significant. The harsh pansystolic murmur of a ventricular septal defect is usually obvious unless the defect is very large. In this case the patient would be likely to have more pronounced symptoms.

Patent foramen ovale

Patent foramen ovale occurs in 10% of the population and is found in 40% of patients with a past history of stroke. If these defects are found in patients with a past history of a cerebrovascular accident, a right to left shunt must be looked for by injecting agitated saline and asking the patient to perform a Valsalva manoeuvre. If a significant right to left shunt is demonstrated, then either long-term anticoagulation or percutaneous closure is recommended, as there is a risk of paradoxical embolus. The results of ongoing studies should help determine whether percutaneous closure is superior to anticoagulation alone in this context. When seen as an incidental finding in patients without a history of stroke, no treatment is required.

Reference

• Martin F. Percutaneous transcatheter closure of patent foramen ovale in patients with paradoxical embolism. Circulation 2002; 106: 1034-6.

Atrial Septal Defect (ASD)

Fig1: Atrial Septal Defect

Fig 2: Atrial Septal Defect.

Eighty-five per cent of ASDs are of the secundum type, 11% of the primum type and 4% sinus venosus defects involving the inferior vena cava (IVC) or superior vena cava (SVC).

Fig 3:
SVASD = Sinus Venosus Atrial Septal Defect;
OSASD = Ostium Secundum Atrial Septal Defect;
OPASD = Ostium Primum Atrial Septal Defect.

Clinical signs are rarely present. When people present in middle age with symptoms this usually relates to the development of progressive pulmonary vascular disease, pulmonary arterial hypertrophy and a change in the direction of flow across the shunt (left to right changes to right to left).

Many ASDs are now being closed using percutaneous closure devices.

Fig 4: ASD Closure

Fig 5: Percutaneous Closure Device (Core-Helex)

Source: Fig 1, Fig 2, Fig 3, Fig 4, Fig 5

Wolf-Parkinson-White Syndrome

Wolf-Parkinson-White is the syndrome of pre-excitation secondary to antegrade conduction down an accessory pathway from atrium to ventricle. This is characterized on the 12-lead surface ECG by a short PR interval, a delta wave and broad complexes (as a result of the delta wave). The accessory pathway can be in any location around the atrioventricular valves, i.e. mitral or tricuspid valves. Using various algorithms it is possible to accurately locate the position of the accessory pathway.

In this patient's case there is a dominantly upright QRS deflection in the right praecordial leads, resulting in tall R waves in leads V1 and V2. This is the picture of Type A WPW, where pre-excitation is usually of the left ventricle.

Lown-Ganon-Levine syndrome differs from Wolf-Parkinson-White syndrome in that it has a short PR interval without a delta wave. This is thought to be due to accessory conduction tissue from the atria to the atrioventricular node. Whilst the complexes are broad, this is clearly sinus rhythm and not ventriuclar tachcardia.