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Myocardial diseases

Mobilisation to be encouraged in viral myocarditis

Which viruses have been implicated in viral myocarditis?

The typical ones are said to be Coxsackie and echo viruses but it is not always easy to get a meaningful result.

What are the presentation, management and prognosis of patients with viral myocarditis?

This can be very varied and any age can be affected. At one extreme a patient can present with severe pulmonary oedema, hypotension, marked tachycardia and gallop rhythm. At the other extreme you could have a patient with just a viral type of myalgia but on ECG you see T-wave changes. You may also get a mixture of pericarditis and myocarditis. It is possible that many of us when we get viral infections get some subtle myocardial inflammation.

Severe cases with pulmonary oedema would have an initial chest X-ray, ECG and standard LVF treatment of oxygen and IV diuretics. An ACE inhibitor would be given once the acute pulmonary oedema was settling. Nitrates can be helpful. All patients would subsequently have an echocardiogram. This usually shows a globally dilated heart with a poor ejection fraction. We would encourage mobilisation to avoid compounding their symptoms with skeletal muscle weakness and to reduce the thromboembolic risk.

In a very small number of patients heart transplantation may be the only option. Rarely, external pumping devices may be used either to support the heart prior to transplant or simply to rest the heart and give it a chance to recover.

For most patients the prognosis is good.

Managing hypertrophic obstructive myocardopathy

What are the prevalence, diagnosis and current treatments of hypertrophic obstructive cardiomyopathy?

Studies show a large variation from one in 500 to one in 5,000 in an ECG and echocardiogram-screened population. In a district hospital we may see one or two new diagnoses per year. Often there are no symptoms but occasionally dyspnoea, exertional or atypical chest pains, faints and palpitations can occur. The worst risk is sudden death, usually associated with arrhythmia.

On auscultation an ejection systolic murmur very similar to aortic stenosis is normally present. The cause is the septum and anterior mitral valve leaflet coming together, in effect producing a sub-aortic stenosis. The character of the pulse is, however, different. In HOCM it is described as 'jerky' whereas in aortic stenosis it is typically a 'slow rising' pulse.

The ECG in HOCM can look weird, with features of marked LVH along with

Q-waves in the septal leads, and looks like serious hypertension or valve disease. The echocardiogram is diagnostic as discussed earlier.

Many patients with HOCM have a good prognosis. Many papers in the past came from tertiary referral centres and tended to look at the more severe end of the spectrum. A few years ago an Italian study looked at sportsmen and women who were screened for HOCM. Those found to have the disease were questioned and followed up and many were found to be asymptomatic and remained so. Ideally you want to identify HOCM patients who are most at risk.

Higher risk factors include a family history of sudden death, atrial fibrillation, a 24-hour ECG tape showing runs of ventricular tachycardia and finally an exercise test showing a drop in blood pressure.

Many patients require no treatment. In symptomatic patients the drugs have traditionally been calcium antagonists or

?-blockers often given speculatively, sometimes for the presence of angina-type pain. Atrial fibrillation should be treated including anticoagulation, amiodarone or cardioversion. In more severe patients, other treatments include pacing to maintain sinus rhythm, implantable defibrillation and removal of part of the septum. A less common technique is alcohol ablation of the septum via a balloon cardiac catheter. This causes a septal infarct with necrosis.

Managing the commoner cardiomyopathies

Is the presentation of primary cardiomyopathy any different from secondary dilated cardiomyopathy due to ischaemic heart disease, hypertension or valvular disease?

All can present with heart failure. Find out if there is any history of previous ischaemia, hypertension, valvular disease or excessive alcohol intake. The resting ECG can be helpful. With heart failure due to myocardial infarction the presence of Q waves, ST segment and T wave changes can increase the likelihood of that diagnosis. With heart failure due to hypertension, the ECG may show features of left ventricular hypertrophy such as high amplitude R waves in the lateral chest leads.

With a dilated cardiomyopathy there may be features of left ventricular strain on ECG. These are the same as those of hypertrophy with added ST changes. A finding of atrial fibrillation can add weight to a diagnosis of alcoholic cardiomyopathy.

There may be secondary mitral regurgitation with a pansystolic murmur due to stretching of the mitral annulus. It is important to recognise that this murmur is the consequence, not the cause, of this type of heart failure.

On chest X-ray a large heart is most likely but in the much rarer restrictive cardiomyopathy the heart can appear small despite obvious heart failure.

What about echocardiogram appearances of the various types of primary and secondary cardiomyopathy?

The echocardiogram is a key investigation in many of these diseases. HOCM has a typical feature of a thickened septum, the so-called 'asymmetric septal hypertrophy', where the septum is thickened out of proportion to the posterior wall of the heart. HOCM can also produce a systolic anterior motion of the mitral valve, bringing it nearer the thickened septum. A symmetrically thickened heart muscle is most often caused by hypertension but there is a cardiomyopathy known just as hypertrophic, without obstruction. Just to confuse matters, top athletes can also show these features due to high training levels.

With a dilated cardiomyopathy you will see a dilated left ventricle. If the cause is an ischaemic heart post-MI, the dilation is often segmental where the infarct occurred.

How are primary dilated cardiomyopathies managed?

Management of the heart failure is similar to that caused by infarct or hypertension. Diuretics are a mainstay, plus an ACE inhibitor and titrating up to an optimal dose.

Nowadays one would consider adding a ?-blocker licensed for use in heart failure such as bisoprolol, metoprolol and carvedilol. If atrial fibrillation is present the patient should be anticoagulated. If the problem becomes worse spironolactone, at 25-50mg daily, could be considered. In primary dilated diseases, lipid levels and statins are not important assuming ischaemic heart disease has been excluded.

How can GPs help to reduce the incidence of the commoner cardiomyopathies and which drugs have the strongest evidence base?

The prevention of both hypertensive and ischaemic heart failure is centered on primary care screening, monitoring and treatment of high-risk patients. Hypertension should be treated. Lipid lowering is of proven benefit. Smoking cessation is vital. We now recognise that the aggressive treatment of risk factors and use of low-dose aspirin in diabetic patients are vital as this group has a much higher risk of ischaemic heart disease. Although positive evidence for the benefits of statins and low-dose aspirin is lacking in over-75s, most specialists would still recommend their use unless future evidence proves otherwise.

Although we hope to see a reduction over the next decade or two we should bear in mind that we are all living longer. It is possible that that we may simply see a shift in the age of the population presenting with heart failure.

The effect of alcohol on the myocardium

How would you make a diagnosis of alcoholic cardiomyopathy?

The presentation would be along the same lines as any heart failure such as breathlessness, fatigue and ankle oedema. One differentiation may be the rhythm change; atrial fibrillation can be a marker. You can get what used to be called the 'holiday heart' where patients went away and binge drank, ending up in atrial fibrillation.

Alcohol, by depressing the myocardium, can also make heart failure from other causes worse. The history is very important, although patients may not volunteer the information or may understate their level of consumption.

One would also look at the past history to exclude other problems such as ischaemia, hypertension or valve disease.

Then of course examination and investigations may also provide clues. Examination may detect some of the obvious signs of alcohol abuse. The rise in MCV and gamma GTT are also helpful indicators.

If a patient with alcoholic cardiomyopathy stops drinking, what effect would this have on prognosis?

Prognosis would clearly improve for some patients. As with most of the risk factors for myocardial disease, one is hoping to prevent the disease getting worse rather than expecting it to reverse.

However, given that alcohol not only produces chronic changes but is also an acute depressant of the myocardium, one would hope to see some reversal in the symptoms and improvement of function in a proportion of patients.

What are the causes of myocardial disease?

How are myocardial diseases currently categorised?

Chronic myocardial diseases are generally categorised according to their underlying pathology. Most myocardial disease we see today is ischaemic, caused by myocardial damage from coronary thrombosis.

The second commonest cause is that related to hypertension even though hypertension is now treated more aggressively. The third group, which is decreasing, is patients with heart valve diseases who usually have congenital heart disease such as aortic stenosis. Next the cardiomyopathies, which are basically heart muscle disorders unrelated to any of the above. They are relatively less common, but need to be recognised when they do occur. Finally there is myocarditis, which is also uncommon.

Which types of cardiomyopathy are most commonly seen in primary care?

Accepting that cardiomyopathies are not common, primary dilated cardiomyopathies are seen most often. These may have a known cause such as alcohol or be idiopathic. They account for between one in 25 and one in 50 cases of heart failure. They present with left ventricular failure initially, sometimes leading to congestive cardiac failure. Next comes hypertrophic obstructive cardiomyopathy (HOCM).

There is also 'restrictive' cardiomyopathy, due to endomyocardial stiffening; amyloid can be one cause. Here the problem is poor diastolic relaxation. An even rarer cardiomyopathy is arrhythmogenic right ventricular cardiomyopathy (ARVC).

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