CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 3, April 2012
AFRICA
137
underlying structural heart disease were included in the impure
TIC group and analysed separately. Patients with a diagnosis of
hypertension were included in the impure TIC group.
The cohort of 33 patients with pure TIC was compared to 12
patients with impure TIC. We were able to compare 25 patients
with pure TIC with 25 control patients with DCMO (matched
for age, gender and presenting LVEF) with regard to clinical,
electrocardiographic and echocardiographic parameters. The
DCMO patients were obtained from the CMO registry at Groote
Schuur Hospital (unpublished data).
To assess for persistence of adverse LV remodelling after
recovery of LV function, the last available echocardiograms
of 17 patients with pure TIC who had recovered LV function
(post-treatment LVEF
≥
50%) were compared to normal
echocardiograms of 17 patients matched for age and LVEF. For
the purposes of this article, TIC includes pure and impure TIC
unless otherwise specified.
Retrospective data collection included clinical,
electrocardiographic and echocardiographic characteristics and
long-term follow up of patients diagnosed with pure or impure
TIC and matched DCMO controls. Patients’ clinical records
were extensively reviewed. All previous electrocardiograms
(ECGs) of patients with TIC were retrieved from an ECG
archival system (MUSE CV system) and reviewed to calculate
mean heart rate prior to the diagnosis of TIC. All 24-hour Holter
monitors performed prior to and at the time of the diagnosis of
TIC were analysed to determine mean and maximum heart rates
during a 24-hour period.
Transthoracic echocardiography was performed to measure
LVEF, left ventricular internal diameter in diastole (LVIDd),
left ventricular internal diameter in systole (LVIDs), left atrial
(LA) size, and to quantitate the severity of mitral regurgitation
(MR) using standard M-mode or modified Simpson’s method
according to the recommendations of the American Society of
Echocardiography. Radionucleotide imaging that calculated
LVEF was used when available. Serial echocardiograms, if
available, were reviewed in patients with TIC to assess the rate
and magnitude of LV functional improvement. All subsequent
visits were reviewed and recurrences of any tachycardias were
documented. Patients who had been discharged to follow
up or who were no longer attending the cardiac clinic were
telephonically contacted.
The choice of treatment of the causative tachycardia was at
the discretion of the attending cardiologist. Generally, in patients
with atrial fibrillation (AF), rate control using atrio-ventricular
(AV) nodal blockers (beta-blockers, calcium channel blockers),
anti-arrhythmic drugs or Digoxin was initially preferred.
Patients with drug-resistant AF who continued to have poor
rate control despite the above treatment, were referred for
AV node ablation (AVNA) and permanent pacemaker (PPM)
implantation. Catheter ablation was considered first-line therapy
for certain arrhythmias [atrial flutter (AFL), atrial tachycardia
(AT), atrio-ventricular nodal re-entry tachycardia (AVNRT),
atrio-ventricular re-entry tachycardia (AVRT) and fascicular
ventricular tachycardia (VT)].
Statistical analysis
Results are expressed as mean (standard deviation) or
median (interquartile range). Clinical and socio-demographic
characteristics of the groups studied were compared using the
Student’s
t
-test, Chi-square test, Mann-Whitney test or Wilcoxon
signed rank test, whichever was appropriate. A
p
-value of < 0.05
was considered significant. Non-parametric tests were used due
to the non-normality of some of the variables studied. Receiver
operating characteristic (ROC) curves were plotted to examine
the diagnostic utility of some variables, which was expressed as
an area under the curve and measured using the
C
-statistic. Data
were analysed using SPSS version 17 (Chicago, Illinois; 2009).
Results
Patient demographics, clinical features, investigations, treatment
and long-term outcomes of the pure and impure TIC cohort are
displayed in Table 1.
The pure TIC cohort consisted of 33 patients (25 males, eight
females). The median age was 44 (30–62) years with a marked
male predominance (76%). Twenty-one (64%) patients presented
with severe effort intolerance [New York Heart Association
(NYHA) class III, IV]. The median duration of dyspnoea and
palpitations prior to presentation was two (0.6–7.5) months
and seven (1.3–51.0) months, respectively. The arrhythmic
causes were AF (
n
= 20), AFL (
n
= 7), AT (
n
= 4), AVNRT
(
n
= 1) and fascicular VT (
n
= 1). The most common ECG
abnormalities were repolarisation abnormalities (55%), followed
by LV hypertrophy (12%) and LA hypertrophy (9%). Q waves,
left bundle branch block (LBBB) and right bundle branch
block (RBBB) were seen in less than 7% of presenting ECGs.
The mean LVEF at presentation was 32.4 ± 9.5%. The mean
LVIDd and LVIDs dimensions were 5.7 ± 0.7 and 4.8 ± 0.8 cm,
respectively. The mean LA size was 4.2 ± 1.0 cm.
The impure TIC cohort consisted of 12 patients (nine males,
three females). Patients had a history of hypertension (
n
=
3), viral myocarditis (
n
= 2), valvular heart disease (
n
= 3),
ischaemic heart disease (
n
= 2), patent ductus arteriosus (
n
= 1)
and peripartum cardiomyopathy (
n
= 1). The median age was 39
(23–59) years with a marked male predominance (75%). Eleven
(92%) patients presented with severe effort intolerance (NYHA
III, IV). The median duration of dyspnoea and palpitations prior
to presentation was 0.5 (0.2–2.0) months and 3 (0.6–4.5) months,
respectively. The arrhythmic causes were AF (
n
= 5), AFL (
n
=
4), AVNRT (
n
= 2) and AVRT (
n
= 1). The most common ECG
abnormalities were repolarisation abnormalities (70%) and LV
hypertrophy (70%). The mean LVEF at presentation was 29.2 ±
1.0%. The mean LVIDd and LVIDs dimensions were 5.7 ± 1.0
cm and 4.8 ± 0.8 cm, respectively. The mean LA size was 4.8 ±
1.5 cm.
Compared to patients with pure TIC, patients with impure
TIC had shorter durations of dyspnoea (
p
= 0.04) and more
clinical signs of heart failure at presentation (
p
= 0.003).
Patients with impure TIC displayed more ECG features of
underlying structural heart disease [LA hypertrophy (
p
= 0.05),
LV hypertrophy (
p
< 0.001) and larger RV
6
voltages (
p
=
0.04)]. There were no significant differences in presenting
echocardiographic features between the two groups.
In order to identify characteristics that may be useful to
differentiate between pure TIC and DCMO at presentation,
we compared 25 patients with pure TIC with 25 patients with
DCMO, matched for age, gender and LVEF. The clinical,
electrocardiographic and echocardiographic features of the two
groups are displayed in Table 2.
Clinically, pure TIC patients were less symptomatic according
