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International Journal of Obesity (2004) 28, 1118–1123
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PAPER
Left ventricular hypertrophy and QT interval in obesity
and in hypertension: effects of weight loss and of
normalisation of blood pressure
AE Pontiroli1,2*, P Pizzocri1, A Saibene3, A Girola1, D Koprivec1 and G Fragasso4
1
Cattedra di Medicina Interna, Università degli Studi di Milano, Milano, Italy; 2Divisione di Medicina Generale 2, Ospedale
San Paolo, Milano, Italy; 3Divisione di Medicina Interna, Ospedale San Raffaele, Milano, Italy; and 4Divisione di
Cardiologia, Ospedale San Raffaele, Milano, Italy
BACKGROUND: Left ventricular hypertrophy (LVH) and prolonged QT interval at ECG (QTc) are common in both obesity and
arterial hypertension (AH), and are risk factors for cardiovascular disease and sudden death.
METHODS: We compared the frequencies of LVH (ECG criteria) and QTc in obese-AH (n ¼ 41), in normotensive obese (n ¼ 75),
in lean-AH (n ¼ 30), and in lean controls (n ¼ 68) comparable for age and sex; in obese patients, LVH and QTc were evaluated
under basal conditions and 1 y later, that is, after a significant weight loss induced by bariatric surgery.
RESULTS: LVH was more frequent, and QTc was longer, in obese-AH, in normotensive obese, and in lean-AH than in lean
controls; after weight loss, frequency of LVH decreased in obese subjects becoming normotensive (n ¼ 87), not in obese subjects
remaining hypertensive (n ¼ 29), while QTc decreased in all obese subjects.
CONCLUSION: Weight loss can effectively reduce QTc; when concomitant AH disappears, weight loss can also reduce the
prevalence of LVH. In obese patients remaining hypertensive, aggressive pharmacological treatment is therefore indicated to
correct LVH.
International Journal of Obesity (2004) 28, 1118–1123. doi:10.1038/sj.ijo.0802733
Published online 20 July 2004
Keywords: bariatric surgery; gastric banding; left ventricular hypertrophy; QT interval; arterial hypertension; cardiology;
electrocardiogram; sympathetic overactivity; left ventricular mass
Introduction
Obesity is an independent risk factor for cardiovascular
diseases such as arterial hypertension, congestive heart failure, and ischaemic heart disease,1–3 and has been proposed as
a risk factor for ventricular arrhythmias and sudden death.3,4
Left ventricular hypertrophy (LVH), as assessed through
ECG criteria (Cornell voltage–duration product) or through
echocardiography, is frequent in both obesity and arterial
hypertension, especially when obesity and hypertension
coexist.5,6 Prolonged corrected QT interval (QTc) has been
reported in cardiac failure,7 in arterial hypertension, particularly in the presence of LVH,8,9 in ischaemic heart
disease,10,11 and in obesity.12 QTc is an index of physiologi-
*Correspondence: Dr AE Pontiroli, Ospedale San Paolo, Via A Di Rudinı̀ 8,
20142 Milano, Italy.
E-mail: [email protected]
Received 16 July 2003; revised 7 October 2003; accepted 3 November
2003; published online 20 July 2004
cal variability of ventricular repolarisation, and an increase
of QTc is a possible risk factor for ventricular arrhythmias
and sudden death;7 in addition, prolonged QTc is an index
of sympathetic overactivity under several cardiac conditions,13–15 and previous studies have shown that increased
sympathetic activation is present in both obesity and hypertension, particularly when the two conditions co-exist.16
Conflicting evidence suggests that weight loss can decrease
LVH; the oldest papers indicated that weight loss, even when
substantial, does not reduce LVH,17,18 but afterwards it was
reported that even an 8 kg loss could decrease LVH;19,20 however, the number of patients enrolled in these studies was quite
small,17–21 and control subjects were not included. In the largest study published so far, 41 surgery operated patients had
weight loss, reduced systolic and diastolic blood pressure, and
reduced LVH; 31 diet-treated patients had no reduction in
either body weight, blood pressure, or LVH.22 Therefore, it is not
possible to conclude that weight loss per se or decrease in arterial
blood pressure per se was the key factor in decreasing LVH.
Obesity, hypertension, LVH, QT interval
AE Pontiroli et al
1119
Only a few studies analysed the effects of weight loss on
QTc, yielding conflicting results:23–30 prolongation of QTc or
sudden death has been reported with very low calorie diets
(VLCD),24–27 while shortening of QTc has been reported with
low calorie diet (LCD).23,28,30
Bariatric surgery appears the treatment of choice for
subjects with morbid (grade 3) obesity, as it allows a
consistent and long-lasting weight loss,31 and a significant
improvement of metabolic profile, associated to a significant
reduction of arterial blood pressure in the majority of
subjects.32
This study was aimed at evaluating the effect of morbid
obesity and of hypertension, and the effect of decrease in
body weight alone, or accompanied by decrease in arterial
blood pressure, on LVH, an index of anatomical deterioration of the left ventricle, and on QTc, an index of
sympathetic overatcivity.
Patients and methods
Obese patients
Obese patients were in a protocol of bariatric surgery
(laparoscopic adjustable gastric banding, LAGB) for morbid
obesity.32,33 The protocol of the study was approved by the
local Ethics Committee. In all, 116 consecutive (20 men, 96
women) obese patients aged 42.070.88 y (mean7s.e., age
limits 22–66 y), BMI 45.170.61 kg/m2 (limits 35–69 kg/m2)
were evaluated under basal conditions and 1 y after bariatric
surgery associated with LCD (900 kcal/day for women and
1100 kcal/day for men; 40% protein, 25% fat, and 35%
carbohydrate). All subjects underwent an oral glucose
tolerance test (OGTT; Alberti and Zimmet34) to detect
diabetes mellitus under basal conditions and, 1 y later, with
determination of insulin and blood glucose levels32 and
calculation of the HOMA index of insulin resistance;35
anthropometric evaluation included waist circumference
and ultrasound evaluation of visceral and subcutaneous
fat.36 In all, 41 patients (8 men and 33 women) were affected
by hypertension. Only patients without any evidence of
Table 1
cardiac disease, according to past history, clinical conditions,
and electrocardiographic assessment, and not using drugs
known to affect QTc, were considered. As part of the
program, serum electrolytes were routinely evaluated (sodium, potassium, calcium, magnesium, and phosphate)
under basal conditions and during follow-up. During the
1-y follow-up study, obese hypertensive subjects were
instructed to continue their antihypertensive treatment
unaltered unless symptomatic hypotension (withdrawal of
treatment) or worsening of arterial hypertension (increase
of treatment) occurred.
Control subjects
The control group was made of subjects undergoing routine
ECG (employment, sport medicine, pre-operative assessment
for general surgery). These subjects (98, 16 men, 82 women)
were comparable with obese patients for age (42.271.01 y,
limits 22–66 y) and sex, and had BMI 22.270.24 kg/m2
(limits 17–26 kg/m2); 30 subjects (five men and 25 women)
were affected by hypertension, while no subject was affected
by diabetes mellitus. As for obese patients, only patients
without any evidence of cardiac disease, according to past
history, clinical conditions and electrocardiographic assessment, and not using drugs known to affect QTc, were
considered.
ECG
ECG in both groups was carried out after an overnight fast
and rest, and on the same occasion arterial blood pressure
was evaluated by the same physician, using the same
sphygmomanometer with an appropriate cuff. Arterial
hypertension was assumed when systolic/diastolic blood
pressure was 4140/90 mmHg, or when subjects were under
antihypertensive treatment. Clinical and ECG characteristics
of the two groups are shown in Table 1.
Clinical and ECG data of subjects in the study
N (M/F)
Age (y)
BMI (kg/m2)
Obesity duration (y)
Systolic BP (mmHg)
Diastolic BP (mmHg)
CVP (mm ms)
QRS (ms)
RaVL (mm)
SV3 (mm)
QTc (ms)
Obese-AH
Obese
Lean-AH
Lean controls
41 (8/33)
48.371.38
46.271.04
27.671.41
142.572.2c
89.571.41c
1814.8792.54c
101.972.98c,d
6.270.52c
7.270.50
416.574.31c
75 (12/63)
38.570.94a
44.570.76
19.870.97a
127.770.87a
80.970.71a
1624.7759.59c
98.171.82c
5.470.36c
6.470.41d
414.373.24c
30 (5/25)
49.371.72
22.970.43
F
147.771.66c
89.970.98c
1729.27113.61c
90.772.24
4.170.62
9.870.99
416.274.68c
68 (11/57)
39.171.04b
21.970.31
F
126.471.36
83.170.94
1330.5754.06
87.171.31
3.470.31
6.970.42d
403.773.45
Means7s.e. or absolute frequencies. AH ¼ arterial hypertension. aPo0.01 vs obese-AH. bPo0.01 vs lean-AH. cPo0.05 or less vs controls. dPo0.05 vs lean-AH.
CVP ¼ Cornell voltage–duration product.
International Journal of Obesity
Obesity, hypertension, LVH, QT interval
AE Pontiroli et al
1120
Left ventricular mass and LVH
Left ventricular mass (LVM) was calculated, through ECG
reading,
as
Cornell
voltage–duration
product
((RaVL þ SV3) QRS in mm ms, with an adjustment of 6 mm
in women)). These composite ECG criteria detect LVH with
about 95% specificity in healthy people and above 70%
sensitivity in obese and in hypertensive subjects.37–39 In
addition, this approach allows direct evaluation of LVM.40–42
LVH was assumed for measures of LVM above 1713 mm ms in
women and above 2440 mm ms in men.37
QTc interval
QT intervals were measured manually from the onset of the
interval between Q and S waves of the electrocardiogram to
the end of the T wave on the isoelectric baseline, and
corrected according to Bazett’s formula (QTc ¼ QT/ORR).43
When a T wave could not be reliably determined, the lead
was excluded from analysis.44 QT interval was measured in at
least 10 leads in each subject.
Statistical analysis
Inter-group comparisons were performed by one-way analysis of variance (ANOVA), followed by Scheffè’s multiple
comparison test. Intra-group comparisons were performed
by two-tailed Student’s t-test for paired samples. The
frequency of LVH was compared by w2. Pairwise correlation
was also calculated between changes of clinical conditions
and change of LVM in obese subjects undergoing weight loss.
Po0.05 was considered statistically significant.
Table 2
Results
Table 1 shows the clinical and ECG data of obese and control
subjects, divided into normotensive and hypertensive. In
both groups, hypertensive subjects were older than normotensive subjects. Serum electrolytes were always within
normal values (not shown). Cornell voltage–duration product and QTc were longer in obese-AH, obese, and lean-AH
than in lean controls; the difference of Cornell voltage–
duration product was due to longer QRS duration and higher
RaVL, while SV3 was higher in lean-AH than in normotensive
obese and in controls. These results did not change when
obese diabetic patients (n ¼ 12) were excluded from calculations.
During the follow-up period, three obese normotensive
subjects became hypertensive, while 15 previously hypertensive subjects became normotensive, so that the number of
normotensive subjects increased by 12. Subjects with
diabetes mellitus declined during the follow-up period from
6 to 3 in the former group and from 6 to 2 in the latter group;
waist circumference, visceral and subcutaneous fat, insulin
levels, and HOMA decreased to the same extent in both
groups.
Table 2 shows changes of clinical and ECG data of obese
patients who were normo- or hypertensive 1 y after bariatric
surgery, that is, after slimming; in the 87 subjects normotensive after 1 y (either since the beginning or becoming
normotensive during the 1-y follow-up) a significant decrease in Cornell voltage–duration product was found,
together with a significant decrease in SV3 voltage; in the
29 subjects hypertensive after 1 y (either since the beginning
or becoming hypertensive during the 1-y follow-up), no
significant change occurred, so that Cornell voltage–duration product was higher than in lean controls. In contrast,
QTc decreased in both groups of subjects. After weight loss,
Clinical and ECG data of subjects undergoing bariatric surgery at baseline and at 1-y follow-up
Obese normotensive
Baseline
N (M/F)
age (y)
BMI (kg/m2)
Obesity duration (y)
Waist circumference (cm)
Ultrasound visceral fat (mm)
Ultrasound subcutaneous fat (mm)
Fasting insulin (mU/ml)
HOMA
Systolic BP (mmHg)
Diastolic BP (mmHg)
Cornell voltage–duration product (mm ms)
QRS (ms)
RaVL (mm)
SV3 (mm)
QTc (ms)
87 (16/71)
39.870.95a
44.870.74
20.570.92a
122.171.59
85.472.91
48.571.13
17.971.11
4.770.66
131.871.36
83.170.91
1678.1755.78
99.371.78
5.670.35
6.570.34
413.472.85
Obese hypertensive
Follow-up
36.570.59
Baseline
b
107.571.58b
48.272.53b
39.271.13b
9.970.55b
2.370.14b
128.871.19b
80.970.82b
1554.7761.38b
96.572.21
5.570.33
5.870.39b
398.072.86b
29 (4/25)
48.971.54
46.170.93
28.971.65
126.671.94
91.475.15
52.671.87
20.272.92
6.270.98
137.172.12
86.971.38
1732.17118.31
99.273.29
5.770.57
7.270.80
420.375.86
Follow-up
38.170.88b
110.871.95b
60.675.18
37.371.71b
10.571.23b
2.770.32b
135.972.47c
86.671.54c
1701.17113.68c
96.273.12
5.170.57
7.870.54
403.875.46b
Subjects are divided according to arterial blood pressure at 1-y follow-up. Means7s.e. or absolute frequencies. aPo0.05 vs controls. bPo0.05 vs baseline. cPo0.01 vs
obese-AH. HOMA ¼ insulin (mU/ml) glucose (mmol/l)/22.5.35
International Journal of Obesity
Obesity, hypertension, LVH, QT interval
AE Pontiroli et al
1121
no changes were observed in serum electrolytes (Na, K, Ca,
Mg, P, not shown). The decrease in Cornell voltage–duration
product was proportional to its initial value (r ¼ 0.357,
P ¼ 0.0001).
BMI decrease after surgery was not different in the two
groups of subjects; the only clinical data that correlated with
decrease in Cornell voltage–duration product was decrease in
diastolic blood pressure (r ¼ 0.186, Po0.05); decreases in
BMI, waist circumference, visceral and subcutaneous fat,
insulin, and HOMA were not correlated. These results did
not change when diabetic patients were excluded from
calculations.
Figure 1 shows the prevalence of LVH in the four groups of
subjects at baseline; among obese subjects re-evaluated after
1 y, prevalence of LVH decreased from 29 to 21 in subjects
who were normotensive, and increased from 8 to 13 in
subjects who were hypertensive (w2 ¼ 9.118, P ¼ 0.0025)
(Figure 2).
Discussion
In this study, Cornell voltage–duration product and QTc
were higher in morbidly obese subjects, with or without
hypertension, and in lean hypertensive subjects than in lean
controls; as a consequence, LVH was more frequent in
morbidly obese subjects, with or without hypertension, and
in lean hypertensive subjects than in lean controls. These
data agree with previous studies showing that obesity and
hypertension are a cause of increased frequency of LVH and
are associated with sympathetic overactivity.5,6,13–16,39,42
Sustained and prolonged haemodynamic burden is required to induce structural changes of the left ventricle as it
happens in long-lasting obesity and in hypertension; a
different explanation might be valid for prolonged QTc, an
index of sympathetic overactivity, a situation which is
present in both obesity and hypertension, especially when
the two conditions co-exist.16
During the 1-y follow-up, obese patients lost a significant
amount of body weight due to bariatric surgery and lowcalorie diet. This weight loss was associated with a significant
shortening of QTc in all subjects, in agreement with previous
studies in which decrease in body weight was obtained
through a low-calorie diet for a prolonged period of
time.23,28,30
Cornell voltage–duration product decreased in subjects
who, after 1 y, were normotensive, but not in subjects who,
after 1 y, were hypertensive. As a consequence, prevalence of
LVH decreased in the first group and increased in the second
group. The decrease in Cornell voltage–duration product was
due to a significant reduction of SV3, and due to a
nonsignificant shortening of QRS, similar in the two groups.
This finding supports and expands previous studies, obtained through echocardiography,21,22 in which the prevalence of LVH decreased through reduction of body weight
and normalisation of blood pressure. In older studies, which
report conflicting results as to LVH, blood pressure was not
considered.17,20
Therefore, we propose that weight loss has a different
effect on QTc and on LVH, depending on the disappearance
or persistence of hypertension.
Sympathetic activation contributes to obesity-induced
hypertension; recent observations suggest that leptin and
its multiple interactions with other neurochemical pathways
in the hypothalamus45 may represent a partial link between
excess weight gain and increased sympathetic activity;42,43
leptin is reduced after weight loss,46 and at least two studies
have shown a positive effect of body weight reduction on
sympathetic nerve traffic.47,48
For LVH a different explanation is possible; subjects with
increased prevalence of LVH at 1 y were older, were
hypertensive, and had a longer duration of obesity, and
hypertension5,6,39,42 and duration of obesity49 are risk factors
Figure 2 Change in frequency of LVH in obese subjects after bariatric
Figure 1 Frequency of LVH in the four groups of subjects in the study.
surgery, according to arterial blood pressure at follow-up.
International Journal of Obesity
Obesity, hypertension, LVH, QT interval
AE Pontiroli et al
1122
for LVH. Reversibility of hypertension is possible with
prolonged treatment with various antihypertensive drugs
that lead to sustained reduction of the haemodynamic
impact;50 Fagerberg et al51 found that reduced sodium intake
coupled with reduced energy intake is more effective than
reduced energy intake alone in reducing blood pressure in
obese-hypertensive patients; finally, we should recall that,
with all surgical techniques such as bilio-pancreatic diversion, gastric by pass, and gastric banding, many subjects
remain hypertensive, whatever the amount of weight
loss;32,52–54 even more important, in the Swedish obesity
study it was shown that surgery does not prevent development of arterial hypertension.55 At present, there is only one
long-term study showing that, in spite of these limitations,
all-cause mortality and cardiovascular mortality are lower in
obese subjects with weight loss due to bariatric surgery than
in subjects remaining obese.56
Study limitations
First, the method we used, highly referenced, does not allow
direct comparisons with data obtained through echocardiography. However, the trends indicated by our data support
and expand previous observations.21,22
Second, it might be that with a more prolonged follow-up,
and with a more aggressive antihypertensive treatment, we
could observe decrease in blood pressure and/or of LVH also
in the group of 29 subjects who remained hypertensive after
1 y, but we have chosen the 1-y interval to compare with the
majority of studies performed so far. A more detailed answer
to the latter question will probably come from a longer
follow-up (7 y), which is under way at our institutions.
Conclusions
Effective weight loss can significantly reduce QTc, indicating
a better control of sympathetic activity. When concomitant
hypertension disappears, weight loss also reduces LVH. As a
consequence, in patients remaining hypertensive, aggressive
pharmacological treatment is indicated to correct LVH.
Acknowledgements
This research was supported by Grant FIRST 2002 from the
Università degli Studi di Milano, from Ministero dell’Università e della Ricerca Scientifica e Tecnologica 2002 (grant
2002064582_003), and from Ministero della Salute (grant
199/02).
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