Fig. 10.1
Electrocardiogram
Fig. 10.2
Chest X-ray
Fig. 10.3
Blood test
10.2 Tests
10.2.1 12 Lead ECG (Fig. 10.1)
Report
Absence of regular atrial activity. Irregular and abnormally elevated ventricular rate, i.e. 147 /min: [normal value of heart rate: 50–100 /min]. Normal QRS axis: +60°. Abnormal QRS prolongation (110 ms), with repolarisation abnormalities compatible with incomplete left bundle branch block (LBBB) (Table 10.1).
Table 10.1
The criteria to diagnose a LBBB on the ECG
The heart rhythm must be supraventricular in origin |
The QRS duration must be ≥ 120 ms |
There should be a QS or RS complex in lead V1 |
There should be a monophasic R wave in leads I and V6 |
The T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischaemia or myocardial infarction |
In our case: QRS duration was 110 ms, so the diagnosis of incomplete LBBB. T wave was concordant suggesting ischaemia.
In conclusion: Atrial fibrillation with elevated heart rate response. Ventricular repolarisation compatible with left ventricular overload / subendocardial ischaemia.
10.2.2 Chest X-Ray Anterior-Posterior View (Fig. 10.2)
Report
Enlarged heart: cardio/thoracic ratio >0.5 (reference value [r.v.] < 0.5); bilateral pulmonary congestion; bilateral pleural fluid accumulation
10.2.3 Blood Test (Fig. 10.3)
Report
Normal haemoglobin level, mild kidney dysfunction (creatinine and nitrogen elevation), electrolyte concentration reduction, elevated values of BNP, normal values of cardiac enzymes.
10.2.4 Echocardiography-2D Parasternal View (Fig. 10.4)
Fig. 10.4
On the left, bi-dimensional (2D)-mode long-axis views in systole and diastole; on the right, M-mode views at the level of the ventricles. AV aortic valve, IVS interventricular septum, LA left atrium, LV left ventricle, RV right ventricle
10.2.5 Echocardiography-2D and Colour Doppler, Two-Chamber, Apical View (Fig. 10.5)
Fig. 10.5
Evidence of moderate mitral regurgitation: the presence of colour flow in left atrium during systolic LV contraction, occupying half of the left atrium area, is compatible with significant mitral disease
10.2.6 Echocardiography Parasternal View (Figs. 10.4 and 10.5)
Report
A poorly contracting, enlarged left ventricle is evident [end diastolic diameter 65 mm (r.v. < 45 mm), end systolic diameter 55 mm (r.v. < 35 mm), ejection fraction 28 % (r.v. > 55 %)] with enlarged left atrium (46 mm; r.v. < 40 mm). Instead, normal wall thickness of IVS (9 mm) and posterior wall (8 mm) (r.v. < 11 mm) are present.
Concerning the mitral valve is evident a reduced surface of closure of the leaflets, that associated with enlarged valve annulus causes functional moderate mitral regurgitation.
After hospital admission, the patient was immediately started on furosemide infusion, low-dose beta-blocker, ACE inhibitor, oral anticoagulants and low molecular weight heparin. After 24 h a progressive clinical improvement was evident (reduction of dyspnoea, loss of 4 kg in weight) with disappearance of X-Ray sign of congestion and pleural fluid accumulation.
After clinical stabilisation, it was decided to attempt cardioversion earlier than the recommended 3 weeks of effective anticoagulant therapy, and therefore a transoesophageal echocardiography was performed which excluded the presence of thrombi and thus reduced the thromboembolic risk (Fig. 10.6).
Fig. 10.6
Transoesophageal 2D echo and colour Doppler imaging. On the left, transverse plane, at mid-oesophagus level, four-chamber view with evidence of the left atrium (LA) and ventricle (LV) and mitral valve leaflets (anterior, AL, on the left; posterior, PL, on the right) with regurgitant jet in LA. On the right longitudinal long axis view at upper oesophagus level with the evidence of LA and left appendage, free of thromboembolic structures
Therefore the patient underwent successful electrical cardioversion (Fig. 10.7: post-cardioversion ECG).
Fig. 10.7
Now p wave in front of QRS complex, with the same axis/polarity of the QRS, is present, indicating a regular organised atrial activity, i.e. sinus rhythm. T wave inversion is present in the anterior leads, suggesting a subendocardial ischaemia
10.2.7 Post-cardioversion 12-Lead ECG (Fig. 10.7)
Question 1
Which is the most likely cause of heart failure in this patient?
- 1.
Ischaemic heart disease
- 2.
Idiopathic DCMP
- 3.
Valvular DCMP
- 4.
Tachycardiomyopath
Answer
- 1.
We cannot exclude the possibility of an ischaemic aetiology of the dilated cardiomyopathy, especially if we consider the signs of subendocardial ischaemia in the pre- and post-cardioversion ECG tracing (although these ECG changes are not uncommon after an AF episode).
- 2.
Idiopathic dilated cardiomyopathy cannot be excluded, or in case of the absence of significant severe coronary artery disease, we may consider the past history of hypertension as a potential cause.
- 3.
This seems an unlikely cause of the disease, according to the finding of the echocardiogram.
- 4.
Sustained chronic tachyarrhythmias often cause a deterioration of cardiac function known as tachycardia-induced cardiomyopathy or tachycardiomyopathy. The exact incidence of tachycardia-induced cardiomyopathy in the general population is unknown, but in selected studies of patients with atrial fibrillation, approximately 25 % to 50 % of those with left ventricular dysfunction had some degree of tachycardia-induced cardiomyopathy. It is an important clinical entity due to the high incidence and potential reversibility of the disease process. In a patient with a negative history of ischaemic heart disease, this clinical entity should be considered Fig. 10.8 [2].
Fig. 10.8
Presents the pathophysiology linking atrial fibrillation and heart failure: heart failure may induce atrial remodelling including stretching of the fibres, which may trigger atrial fibrillation (AF). By increasing heart rate (HR) response, AF may determine reduction in cardiac output (CO), renal blood flow (RBF) with compensatory responses (including activation of the angiotensin (AT-II) and catecholamine (CA) systems). These changes induce myocardial fibrosis, beta-receptor downregulation and reduced vasodilating natriuretic peptide (ANP), all factors involved in the pathogenesis of heart failure (Modified from Crijns et al, EHJ 1997)
Before discharge, the patient underwent cardiac catheterisation (Figs. 10.9 and 10.10) including coronary angiogram and left ventriculography, which excluded the presence of significant coronary artery disease but confirmed a poorly functioning dilated left ventricle.
Fig. 10.9
Normal coronary angiogram. LM left main, LAD left anterior descending coronary artery, CA circumflex coronary artery, RCA right coronary artery
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
