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Correlation between the electrocardiogram and the pathological findings in the autopsies of patients with complete left bundle branch block and cardiac failure

Crudo, Norma; Piombo, Alfredo; Parisi, Coloma; Romeo, Ligia; Ramos, Alberto.

Cardiology and Pathology Divisions
Hospital del Gobierno de la Ciudad de Buenos Aires “Cosme Argerich”
Buenos Aires, República Argentina

Material and Methods

Background: Left bundle branch block (LBBB) is associated to a significant increase in mortality regardless of the severity of the underlying heart disease.
Methods: Forty one patients who died during hospital stay with clinical signs of heart failure NYHA class III-IV were included in the study. Twenty six patients had persistent LBBB (group 1) and 15 patients had no evidence of ventricular conduction defects (group 2). Sixteen clinical and anatomic variables were compared between both groups. In group 1 patients QRS axis and 12 ECG criteria were related to necropsy findings.
Results: Group 1 showed, compared to group 2 : 1) heavier hearts (562.8+-133 vs. 446.4+- 124 g) (p<0.01); 2) lower left ventricular shortening fraction (18.8+-3% vs. 23+-7%) (p<0.05); 3) higher prevalence of idiopathic dilated cardiomyopathy (34.6% vs. 6.7%) (p<0.05); 4) thickening of intramyocardial coronary arteries (88% vs. 6.7%) (p<0.00001). Patients with LBBB and QRS axis >= +120º were significantly younger than those with an axis <= -45º (47.2+-6.7 vs. 85+- 15 years) (p<0.05). No macroscopic or microscopic differences were found between both groups in necropsy findings. In regard to ECG analysis, only ST segment and T wave alterations showed good sensitivity (73%) and specificity (100%) for the diagnosis of acute myocardial infarction in the presence of LBBB. The ECG showed low sensitivity for the diagnosis of left ventricular hypertrophy.
Conclusions: Patients with LBBB had : 1) Diffuse ventricular damage without any particular cause to justify the QRS axis shift; 2) Poor predictive power of the ECG criteria to detect an AMI or left ventricular hypertrophy, with the only exception of repolarization changes; 3) Wall thickening of intramural coronary arteries with significant reduction of vascular lumen.



The complete left bundle branch block (LBBB) is rare. LBBB is often related with heart enlargement, coronary artery and/or hypertensive heart disease. LBBB is associated with a significant mortality increase regardless the underlying heart disease.

The aims of the present study are:

1) To describe the cardiac macro- and microscopical pathological findings in autopsies of patients with LBBB during their life.
2) Correlate the electrical axis from QRS complex in the LBBB with: a)Heart weight , b) Severity of the coronary disease and c)Extension of the myocardial damages.To establish the correlation between the electrical QRS axis in cases of LBBB with: a)heart weight; b) the severity of ischemic heart disease and c)the extension of the myocardial damage.
3) To determine the electrocardiographic signs of acute and/or chronic ischemic disorders in cases with ischemic heart disease.
4) State if patients presenting left ventricular hypertrophy at the necropsy already showed signs demonstrating its presence in the ECG.


Material and Methods

From March 1990 to June 1996 we studied 307 autopsies of patients died in our hospital. This study include the autopsies of 41 patients with clinical signs of class III-IV NYHA heart failure. The cases were divided in two groups: Group I. included 26 autopsy cases corresponding to 26 patients presenting 2 or more ECG signs of LBBB, Group II. Included 15 patients with class III-IV NYHA heart failure without ECG signs of LBBB.

The diagnostic criteria of LBBB were:

a)Supraventricular conduction,
b) P-The segment > 0.12 sec.,
c) QRS complex duration > 0.20 sec.,
d)R wave slowed and impasted in DI, V5 and V6 with intrinsicoid deflection > 0.04 seg.

From the pathological study the following points have been considered:

a)Heart’s weight;
b) Enlargment degree in cardiac chambers ;
c) Thikness of : Left ventricular lateral wall and the septum and right ventricular lateral wall at upper, middle and lower level;
d)Coronary arteries with significant obstruction (>70%). According to the protocol each of the coronary arteries has been analyzed at each centimeter of its lenght by determining the degree and characteristics of the obstruction,
e) Type and severity of the valvular injuries;
f)Characteristics and extent of injuries at endocardial, miocardial and epicardial level, both macro- and microscopically;
g) Localization and extent of the acute and or sequelar myocardial infarction.

It has been evaluated nine ECG criteria considered by different authors as diagnostics of acute myocardial infarction and / or previous healed myocardial infarction in patients with LBBB. Nine electrocardiographical criteria have been evaluated by different authors after considering them as acute myocardial infarction and/or sequelar diagnostics in patients presenting LBBB in ECG. T signs have been analyzed in all group 1 patients independently of the underlying pathology .

The presence or absence of each one of this signs has been correlated with the pathological findings; the sensibility and specificity of each sign has also been evaluated.

1.- The notching in the wave R from D1, a VL , V5 and V6 (Chapman and Pearce sign).
2.- Notching >0.04 sec. from the ascending part of the S wave from V3 to V5 (Cabrera and Friedland sign).
3.- Wave Q > 0.04 sec. duration in DI, aVL, V5 and V6.
4.- Primary changes in S-T segment and wave T, with displacement of S-T segment in the same direction of the greater deflection of QRS complex in 2 or more contiguous leads.
5.- Slowness from the first 0.04 sec. of QRS complex with R wave impasted in DII, DIII and aVF.
6.- Q Wave > 0.035 sec in DII, DIII and aVF.
7.- Regression of R wave from VI to V3. Septal myocardial infarct sign.
8.- Pattern QS from VI to V3. Sign of apical myocardial infarction particularly from the paraseptal right area.
9.- Pattern RS with final S wave impasted > 0.04 sec. in V5 - V6. Sign of myocardial infarction from the lateral wall of the left ventricle.

Statistical analysis: The continuous variables have been compared applying Student’s t-test and the discrete variables have also been compared by que chi-square test with Fishers correction if required. The p value under 0.05 has been considered significant.



26 cases were included in group 1. Males 22 and females 4 with ages between 27 and 93 years (mean age 61.3 + 16.6 years). There were no significant differences concerning sex and age in the 15 patients included in group II; 12 of them were males and 3 females with ages between 31 and 84 years (mean age 55.8 + 15.5 years) (Table I).

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The 41 patients included in this study presented during their hospitalization clinical signs of cardiac failure III-IV degree but the patients from group I showed in all electrocardiographic studies realized during hospitalization a greater damage from the cardiac function with a lower fraction of shortening (18.8 + 3.3% vs. 23 + 7.4%) (p < 0.05) and more enlarged auricular and ventricular chambers. The last ones would be related with a greater incidence of idiopathic dilated myocardiopathy between the patients of Group I.

Concerning the underlying pathological etiology from patients included, the coronary artery disease has had a similar prevalence in both groups whereas the idiopathic delated myocardiopathy was five times more frequent between patients of Group I (34.6% vs. 6.6%); (p < 0.05). (Table II).

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Three male patients presented LBBB with QRS electrical axis at frontal level

< -45°. The mean age was 85 + 15 years (68 to 93). The three patients had severe coronary artery disease with significant obstruction of two coronary arteries in one case (right coronary and anterior descending and three coronary arteries in the two remaining cases (right coronary artery, anterior descending and circumflex coronary artery). The heart weight was increased between 570 and 640 gr. (mean: 606.6 + 32.1 gr. ) presenting large myocardial areas with acute and/or sequelar necrotic lesions.

Five male patients with a mean age of 47.2 + 6.7 years (37 to 54) presented LBBB with QRS electrical axis deviated to right > + 120°. Four patients had an idiopathic dilated cardiomyopathy without coronary artery disease, but presenting severe dilatation of atrials and ventricles. Three of this patients died from pulmonary thromboembolism and lung infarction.

Only one patient had a severe coronary disease with a significant obstructive damage of the arteries: right coronary, anterior descending, posterior descending and the main left coronary artery. This patient died from an extensive acute subendocardial anterior myocardial infarction becoming circumferential at the apex. The five patients presented an increased heart weight which mean was 605 + 23.8 gr. (560 to 680).

We have state that at microscopical level in the pathological examination the patients with LBBB and electrical axis deviated to the left as well as the patients with LBBB and electrical axis QRS deviated to the right showed that the injuries affected in the same proportion the totality of the ventricular myocardium. There was no defined area showing greater or minor damage compared with the remainder of the ventricle justifying the electrical axis deviation to < -45° or > 120° in the LBBB.

Comparing the LBBB patients with deviated axis to the left with the LBBB patients with deviated axis to the right we observed that the last ones were significantly younger than the first ones (47.2 + 6.7 vs. 85 + 15 years; p < 0.05). (Table III).

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Based in the pathological examination we observed that 12 patients of the Group 1 and 11patients from group II presented coronary artery disease with significant obstructive lesions of one or more coronary vessels.

At the pathological study 12 patients from group I as well as the 11 patients from Group II presented acute and/or healed necrotic lesions largely affecting left ventricle wall and papillary muscles, causing a severe impairment of the contractile function and the clinical signs of class III-IV NHYA heart failure.

Table IV shows that only ST-T segment had high sensibility (73%) and specificity (100%) to diagnose acute myocardial infarction, while the other electocardiophic criteria showed poorest sensibility and low specificity. The ST > 4 mm deviation toward the greater deflection of QRS complex in more than two precordial contiguous leads with negative T wave was the most sensitive diagnostical ECG sign of acute myocardial infarction. Two patients with anterior acute myocardial infarction presented only negative T wave in VI-V2-V3. According to our observations this was a temporary ECG sign during the acute phase disappearing later showing no QRS abnormalities allowing to make a retrospective myocardial infarction diagnosis.

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Five of seven patients from group I (71%) died according to the pathological study due to acute pulmonary thromboembolism with pulmonary infarction. All of them had ST-T disturbances in the DII-DIII and aVF leads with ST > 4 mm in the same direction as the QRS complex in their last ECG.

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- Pathology:

Patients of Group I showed severe macroscopical and microscopical lesions involving the heart.

A) - Macroscopy:

Patients of Group I had increased heart weight. The patients with idiopathic dilated cardiomiopathy showed the four cardiac chambers very dilated (xxxx/4) with thrombus atrial appendix. Patients of both groups presented an extended necrotic damage of the ventricular myocardium caused by coronary artery disease. 75% of the patients of Group I and 72.7% of the patients of Group II also shown hemorrhages areas and fibrotic areas as a consecuense of acute and chronic transmural and non transmural necrotic lessions. No significant differences have been observed in the number of >70% obstructed coronary vessels and in extention of myocardial necrosis between both groups. Even though Group I patients with coronary disease presented external cardiac rupture in 25%, rupture of the left ventricle anterior papillary muscle in 16.6% as a complication of a large AMI and 50% died from a extensive circumferential subendocardial AMI. Among Group II patients with coronary disease these kind of AMI complications have not been observed.

The endocardium was thickene and whitish, with extensive hemorrhagic areas in most patients with coronary artery disease. The epicardium was also fibrous and thicken and in some cases, with adipose infiltration.

There were not signifficant differences between Group II and Group I patients concerning to the endocardium and epicardium, but the heart weight was lesser (446.4 + 124.03 gr vs. 562.78 + 133.47 gr.; p < 0.01) and in the myocardium there was a prevalence of acute necrotic and hemorrhagic injures over the fibrous tissue in the 63.6% of patients with coronary artery disease.

B) - Microscopy

All patients presented extensive fibrosis of the endocardium and epicardium with leukocytic swelling and infiltration patches.

Group I, as well as group II cases presented myocytic hypertrophy, diffuse interstitial sclerosis micropatches shaped including muscular fibers and extensive areas of myocytlysis with subendocardial predominance. One case in group I had also amyloidotic myocardial depots. As observation to be underlined we point out that the 88.5% of the group 1 cases presented a generalized thickening of the myocardial vessels wall, which was more prominent at left ventricle level. This thickening was produced by fibrosis of the intima and fibromuscular hyperplasia of the media, causing a sharp reduction of the vascular lumen. One of the three cases without myocardial thickening vessels had an extensive chagasic cardiomyopathy and the other two cases showd severe coronary artery disease. On the other hand only one of the cases of group II presented myocardial vessels wall thickening. This case concerned a hypertrophic myocardiopathy and presented a gross hypertrophy of the whole ventricular myocardium (lateral wall left ventricle 2.7 cm and septum 3.5 cm), including myocardial vessels wall thickening. It was observed a very significant statistic difference between group I and group II concerning the number of cases presenting microscopically intramyocardial vessel wall thickening (88.5% vs. 6.7%; p < 0.00001).



Our population was composed predominant by male patients with a big increase in the heart’s weight and clinical signs of NYHA III IV Class heart failure.

This findings were much more important in patients with LBBB who at the pathological study presented a severe heart weight increase (562.78 + 133.47 vs. 446.4 + 124.03 gr.; p < 0.01) and a pronounced damage of the contractile strenght of the left ventricle (shortening fraction 18.8 + 3.3 vs. 23 + 7.4; p < 0.05).

Among the cases with LBBB it was observed a greater prevalence of myocardial disease (34.6% vs. 6.6%) (p< 0.05) as well as more cases of coronary artery disease than in patients without LBBB.

The cases of LBBB and electrical axis deviation to > 120° presented a greater incidence of idiopathic dilated cardiomyopathy with severe heart enlargement and noticeably lower age than the remainder of cases with LBBB at their death.

This observations would identify a high risk group among the cases with LBBB, because those patients developing an electrical axis at > 120° would have a faster evolution towards a pump failure and a greater risk to die earlier than the remaining cases with LBBB.

All patients with LBBB and electrical axis < -45° presented a marked increase of the heart weight and severe coronary disease at their pathological study with extensive acute and chronic necrotic injuries involving the ventricular myocardium nearly in all its extension.

However there were not significant differences at the pathological studies which could be considered as determinants of the differences on the electrical axis from QRS complex concerning the cases with electrical axis > 120°.

We observed that excepting the ST segment and the T wave alterations the diagnostic criteria for the anterior AMI showed a poor sensibility and, in some cases, low specificity.

One of our findings from which we did not have any reference in the literature was that 71% of the cases with LBBB died from chronical pulmonary massive thromboembolism and pulmonary infarction, presenting a ST > 4 mm displacement in the same direction as the larger QRS deflection in DII-DIII and

aVF leads, which would show a rough pressure increase in the pulmonary artery.

In the pathological analysis we verified that all cases presented an extensive damage concerning equally every anatomic heart structures at macro- as well as microscopical level.

Concerning the patients presenting LBBB and electrical axis deviation < -45° and the patients presenting the same deviation but > + 120° no significant differences have been observed concerning the type and extent of the injuries comparing them with the cases with LBBB but with normal axis.

At the totality of cases the ventricular myocardium was severely and massively sick at macro- and microscopical level, without showing areas with greater or lesser damage which could explain the differences in the LBBB electrical axis.

Microscopically 88.5% of the cases presented thickening in the wall of the myocardial vessels with an evident vascular lumen reduction and a highly significant difference (p < 0.00001) concerning the cases without LBBB.

This histoarchitecture alteration observed in cases with LBBB would allow us to conclude that the chronical ischemia provoked by the reduction of the vascular lumen in myocardial vessels is one of the etiological factors of this intraventricular conduction disorder.

The chronic ischemia due to the alteration of the myocardial microcirculation could determine the degenerative alterations of the electrical fibers, thus originating the LBBB.

We have to stand out that wall’s thickening of the myocardial vessels was independent from the hypertrophy presence of the ventricular myocardium because it has been observed included in cases with an important distention of the four cardiac cavities without myocardial fibers hypertrophy signs.

On the other hand this myocardial microcirculation engagement could explain the defects in the Tallium 201 capture during the exercise (shown in the myocardial perfusion studies) of the LBBB patients presenting normal coronary arteries in the coronarography.


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