心电图对冠状动脉病变的定位及预测分析

本文分析了６２例Ｑ波性心肌梗塞（ＭＩ）患者的心电图（ＥＣＧ）与病变冠状动脉及运动异常室壁的关系。结果显示，３３例前壁ＭＩ中，９４％有前降支病变，８２％有左室前壁或心尖部运动异常；３０例下壁ＭＩ中，９０％有右冠状动脉或回旋支病变（右冠状动脉占８９％），７６％有左室下壁运动异常；１０例侧壁ＭＩ中，９０％有前降支病变，７０％有左室前壁或心尖部运动异常。４８例患者可确定梗塞相关动脉，其中前壁ＭＩ对前降支病变定位诊断的预测值为８９％，下壁ＭＩ对右冠状动脉或回旋支病变定位诊断的预测值为７３％。结果表明，ＥＣＧ对Ｑ波性ＭＩ患者病变冠状动脉及运动异常室壁的定位诊断有较高的价值。     

Electrocardiographic prediction of ejection fraction and site of LAD occlusion in anterior myocardial infarction

Q-wave anterior myocardial infarctions due to occlusion of the left anterior descending artery (LAD) are generally associated with the most extensive left ventricular damage. The presence of abnormal Q waves on the electrocardiogram (ECG) provides important information to localize the site of left ventricular infarction. However, the relationship between abnormalities of the QRS morphology in the precordial leads and angiographic information such as ejection fraction and the site of LAD occlusion (before or after the first septal perforator) has not been studied extensively. Seventy-three patients with single-vessel disease with complete LAD occlusion, abnormal QRS morphology in leads V₁-V₄ on ECG, and abnormal wall motion with contrast ventriculography were studied retrospectively. LAD occlusions were proximal to the first septal perforator in 33 patients and distal in 40 patients. Q waves were present in 59 patients, and the other 14 patients had either minimal R waves (<0.25 mm), poor R-wave progression, or R-wave regression. A significantly higher ejection fraction was associated with the presence of R wave in V₂ (0.52 ± 0.18 vs. 0.39 ± 0.15 in the absence of R wave, p<0.003). LAD occlusion after and before the first septal perforator was associated with R wave in V₂ in 67 and 36% of patients, respectively. Sensitivity and specificity of predicting occlusion after the first septal perforator based on R wave in V₂ was 0.68 and 0.64, respectively. In patients with anterior myocardial infarctions, occluded LAD artery, and abnormal QRS morphology in the precordial leads, the presence of R wave in V₂ is a useful predictor of higher ejection fraction. The prediction of site of LAD occlusion in relation to the first septal perforator based on ECG findings is limited and probably not sufficiently specific or sensitive to be of clinical use.     

Ventricular Tachyarrhythmia Associated with Hypertrophic Cardiomyopathy: Incidence,Prognosis, and Relation to Type of Hypertrophy

VT Associated with HCM . Objective: To assess the incidence, characteristics, and prognosis of ventricular tachyarrhythmia in hypertrophic cardiomyopathy (HCM). Patients: The study consisted of 66 consecutive patients with HCM who were admitted to Niigata University Hospital between 1992 and 2005. Their clinical characteristics and ECG morphology were investigated according to the type of HCM. Results: The type of HCM was asymmetric hypertrophy (ASH) in 34 patients (51%), obstructive HCM (HOCM) in 9 (14%), apical HCM (ApHCM) in 14 (21%), and midventricular obstruction (MVO) in 9 (14%). The cause of admission was ventricular tachyarrhythmia in 25 patients (38%), unexplained syncope in 11 (17%), and heart failure in 30 (45%). Sustained monomorphic ventricular tachycardia (SMVT) occurred in 19 patients and ventricular fibrillation in 6. In the 19 patients with SMVT, 12 had MVO and 3 of these had previous apHCM. Six of the 19 patients with SMVT had ASH, and 3 had abnormal apical wall motion. In 14 patients, the SMVT appeared to originate from the apical aneurysm based on the morphology of the tachycardia. Ventricular tachyarrhythmia recurred in 14 of the 25 patients (56%), and 4 of the 18 patients with an ICD had electrical storm. ASH with abnormal wall motion of the LV apex or MVO was recognized in the 4 patients with electrical storm; they commonly had abnormal Q waves and ST elevation in leads V4–V6. Conclusion: Ventricular tachyarrhythmia was responsible for 38% of hospitalizations in HCM, and SMVT occurred in patients with MVO and/or with abnormal wall motion of the LV apex. Electrical storm was more common in patients with ST elevation in precordial leads V4–V6. (J Cardiovasc Electrophysiol, Vol. 21, pp. 991‐999, September 2010)     

Q waves in hypertrophic cardiomyopathy in relation to the distribution and severity of right and left ventricular hypertrophy

The cause of abnormal Q waves in hypertrophic cardiomyopathy remains unclear. Myocardial wall thickness was assessed by two-dimensional echocardiography at 8 left ventricular and 10 right ventricular sites in 67 patients (mean age 40 years) with hypertrophic cardiomyopathy and the findings were analyzed in relation to the presence of abnormal Q waves on the 12 lead rest electrocardiogram (ECG). Nineteen (28%) of the 67 patients had abnormal Q waves. Right ventricular hypertrophy was significantly more common in patients without abnormal Q waves (25 [52%] of 48 versus 2 [11%] of 19, p less than 0.001). With univariate analysis, there were six measurements that were significantly associated with abnormal Q waves: an increase in upper anterior septal thickness (p less than 0.005) and maximal left ventricular wall thickness (p less than 0.02), a decrease in mean and maximal right ventricular wall thickness (both p less than 0.005) and an increase in the ratio of both upper anterior septal to mean right ventricular wall thickness (p less than 0.005) and upper anterior septal to upper posterior wall thickness (p less than 0.005). With multivariate analysis, only the ratios of upper anterior septal to mean right ventricular wall thickness (p less than 0.005) and to upper posterior wall thickness (p less than 0.05) were significantly related to the presence of abnormal Q waves and predicted Q wave location with a sensitivity, specificity and predictive accuracy of 90%, 88% and 89%, respectively. In hypertrophic cardiomyopathy, the presence of abnormal Q waves on the 12 lead ECG is primarily a function of the relation of right ventricular wall thickness and upper anterior septal thickness.     

Interpretation of electrocardiographic abnormalities in hypertrophic cardiomyopathy with cardiac magnetic resonance.

AIMS: To clarify the mechanisms of electrocardiographic abnormalities in hypertrophic cardiomyopathy, 102 patients were examined with cardiac magnetic resonance. Distribution and magnitude of hypertrophy and late-enhancement were correlated with electrocardiographic abnormalities. METHODS AND RESULTS: Abnormal Q waves were associated with greater upper anterior septal thickness (22+/-7 mm vs. 18+/-5 mm, P=0.001) and increased ratios of upper anterior septum to mean inferolateral (P=0.01), anterolateral (P=0.002), apical (P=0.001), and right ventricular (P=0.001) wall thickness. There was no relation between abnormal Q waves and late-enhancement, except for Q waves >/=40 ms (P=0.02). Conduction disturbances and absent septal Q waves were associated with late-enhancement (89 vs. 45%, P=0.01 and 75 vs. 39%, P=0.002, respectively). The depth of negative T waves was related to an increased ratio of the mean thickness between apical and basal level (P=0.01), and to the presence of apical late-enhancement (P=0.03). CONCLUSION: Abnormal Q waves reflect the interrelation between upper anterior septal thickness and other regions of the left and right ventricles, and wider Q waves are associated with late-enhancement. Conduction disturbances and absent septal Q waves are associated with late-enhancement. The depth of negative T waves is related to craniocaudal asymmetry and apical late-enhancement.     

An advanced form of familial hypertrophic cardiomyopathy showing massive myocardial fibrosis with intramural small arterial thickening. An autopsy case

An autopsy case of an advanced form of hypertrophic cardiomyopathy (HCM) showing marked fibrosis with intramural small arterial abnormalities is presented in this report. A 52-year-old woman, who had a positive family history of HCM, was admitted because of palpitations. The chest roentgenogram showed a mildly enlarged cardiac silhouette and the electrocardiogram revealed abnormal Q waves and R wave and T wave abnormalities. The echocardiogram revealed hypokinesis with thinning of the interventricular septum and the anterior wall of the left ventricle. Percutaneous right ventricular endomyocardial biopsies demonstrated moderate interstitial fibrosis with small arterial thickening. At necropsy, the anterior and posterior walls of the left ventricle and the interventricular septum were markedly thinned and showed a massive transmural fibrosis. Moreover, the intramural small arteries, 50-300 microns in diameter, showed marked intimal and medial hypertrophy with proliferation of elastic fibers and smooth muscle cells. From these findings, it is suggested that this was originally a case of HCM which progressed to a decompensated stage because of the abnormal intramural small arteries. The significance of small arterial lesions in HCM is discussed.     

Correlations between electrocardiographic findings and echocardiographic patterns in 116 patients with hypertrophic cardiomyopathy

To evaluate the correlation between electrocardiographic and echocardiographic m-mode (E-TM) and two-dimensional (E-2D) patterns, 116 patients with hypertrophic cardiomyopathy (HCM) were studied by these two methods. Patients were classified into four types, according to Maron et al's E-2D classification of HCM. In addition a subgroup (IIIb) of 15 patients in types III, had typical left ventricular concentric hypertrophy. Twelve per cent of the study patients had a normal ECG, and most often those patients showed types I-II and IIIb. Left ventricular hypertrophy by ECG was most frequent (46%) and was found mostly in type III (P less than 0.02). Abnormal Q waves, suggestive but not diagnostic of HCM, were found in 22 of 116 (18%) patients, and were present in equal proportion in each morphologic type. Isolated ST-T changes were found in the same percentage of patients. Six of 7 patients with giant negative T waves had apical left ventricular hypertrophy, but 4 other patients with apical hypertrophy had no such ECG findings. Mean left atrial dimensions at E-TM, although larger in patients with atrial fibrillation, with statistical significance (P less than 0.001), were not predictive of this arrhythmia. ECG is still useful in the diagnosis of HCM, although there is no abnormal pattern specific for the disease, and even a normal ECG can be found in these patients.     

Inaccuracy of various proposed electrocardiographic criteria in the diagnosis of apical myocardial infarction--a critical review

The diagnostic accuracy of the standard electrocardiogram (ECG) in apical myocardial infarction (MI) was evaluated in 112 consecutive patients with recent MI and wall-motion abnormalities limited to the left ventricular (LV) apex on two-dimensional echocardiography, performed at rest 21 to 84 days after MI. The following patterns of abnormal (greater than or equal to 30 ms) Q waves were found: anteroseptal (Q V1-V4) in 44 patients (39.3%), anterolateral (Q V1-V6 and/or I, aVL) in 22 (19.6%), inferior (Q III, aVF or II, III, aVF) in five (4.5%), lateral (Q I, aVL and/or V5-V6) in five (4.5%), anteroinferior in six (5.3%); non-Q MI was present in 30 patients (26.8%). By applying various proposed ECG criteria, the presence of apical MI was correctly identified in very few (24, 21%) patients. LV apex was extensively asynergic in 85 patients (76%) and partially asynergic in 27 (24%). All the patients with Q waves in lateral leads and 47% of the patients with non-Q MI had partially asynergic LV apex, while in the other ECG patterns, extensively asynergic LV apex was predominant. The presence of both greater than or equal to 30 ms Q waves and loss of R in left precordial leads and I strongly suggests extensive apical asynergy; normal QRS in the same leads, however, does not exclude extensive apical involvement.(ABSTRACT TRUNCATED AT 250 WORDS)     

Multivariate analysis of angiographic, histologic, and electrocardiographic data in patients with coronary heart disease

In 61 consecutive patients undergoing aortocoronary bypass grafting, angiographic and electrocardiographic (ECG) changes were studied. Histologic delineation of myocardium was obtained by analysis of transmural biopsy specimens acquired at the time of surgery. The use of principal-component analysis revealed three definite groups of patients. Group I comprised patients with histologic findings associated with severe left anterior descending coronary artery (LAD) stenosis, without abnormal wall motion or ejection fraction. ECG abnormalities were limited to ST changes. Group II comprised patients with severe myocardial cell degeneration with only modest fibrosis associated with severe LAD stenosis and severely impaired wall motion. The incidence of infarction on the ECG was low. Group III patients had important myocardial cell degeneration with severe fibrosis associated with severe LAD stenosis, severely depressed wall motion, and significantly impaired ejection fraction. In this group there was a high incidence of infarction apparent on the ECG. Postoperative follow-up (24 months) showed a total survival of 94.4% in group I, 92.8% in group II, and only 72.7% in group III. This identification of subtypes of coronary artery disease seems to be helpful in estimating patient prognosis after coronary surgery.     

How epicardial U-wave changes are reflected in body surface precordial electrocardiograms in anterior or inferoposterior myocardial ischaemia during coronary angioplasty.

OBJECTIVES: To examine the epicardial U-wave changes recorded in intracoronary electrocardiograms (ECGs) during anterior or inferoposterior myocardial ischaemia and the corresponding changes in precordial ECGs recorded from the body surface in humans. METHODS: 40 patients undergoing coronary angioplasty of the left anterior descending (LAD) coronary artery (22 patients) or left circumflex (LC) artery (18 patients). Intracoronary and surface precordial ECGs were simultaneously recorded under baseline conditions and during angioplasty. RESULTS: Four different patterns of U-wave change were identified on the intracoronary ECG: change to positivity, no change, change to negativity, and biphasic change. The incidence of each pattern was similar in the two groups (LAD v LC groups, 23% v 39%; 23% v 17%; 41% v 44%; 13% v 0%, respectively). The intracoronary ECG was more sensitive than the surface ECG for detecting U-wave changes (intracoronary v surface ECG: LAD group, 77% v 55%; LC group, 83% v 28%). A study of the correlation between intracoronary and surface precordial ECGs showed that in patients who had U-wave changes in their intracoronary ECG (17 LAD and 15 LC patients) 65% of the LAD group but only 6% of the LC group had primary U-wave changes in the surface precordial ECG, and that 27% of the LC patients had reciprocal U-wave changes in the right to central precordial ECG. CONCLUSIONS: These results provide fundamental information for an understanding of the correlation between U-wave changes in the epicardial and surface pre-cordial ECGs during myocardial ischaemia in humans. As well as the primary U-wave changes seen in many of those with anterior myocardial ischaemia, some of those with posterior myocardial ischaemia had reciprocal U-wave changes in their surface precordial ECGs.     

So-called "ampulla" cardiomyopathy associated with coronary vasospasm compared with acute myocardial infarction showing similar abnormal left ventricular wall motion: two case reports

So-called "ampulla" cardiomyopathy is characterized by transient abnormal left ventricular wall motion showing hypokinesia around the apical area and hyperkinesia at the basal area, without any detectable coronary lesion. We recently treated a patient with "ampulla" cardiomyopathy (Case 1) and a patient with acute myocardial infarction showing similar abnormal left ventricular wall motion (Case 2). A 75-year-old female (Case 1) presented with "ampulla" cardiomyopathy without coronary lesion. Vasospasm was induced at segment 8 on the left anterior descending (LAD) coronary artery by intracoronary administration of acetylcholine. A 58-year-old male (Case 2) presented with acute myocardial infarction due to occlusion at segment 8 and underwent successful coronary reperfusion therapy by direct percutaneous transluminal coronary angioplasty. Both Case 1 and Case 2 revelaed similar abnormal left ventricular wall motion, with hypokinesia around the apical area and hyperkinesia at the basal area by echocardiography, in the acute phase. Furthermore, these two patients showed elevated ST segment at both anterior and inferior leads by electrocardiography, and markedly reduced uptake of beta-methyl-p-iodophenyl-pentadecanoic acid around the apical area in the acute phase by scintigraphy. Interestingly, the LAD perfused a relatively wide area including the anterior, apical and part of the inferior area of the left ventricle in both patients by coronary angiography. The abnormal wall motion of Case 1 disappeared 4 weeks after onset, but that of Case 2 did not disappear. Although the diagnoses of Case 1 and Case 2 were different, abnormal wall motion of these cases might be due to myocardial ischemia due to distal LAD lesion. "Ampulla" cardiomyopathy might develop from transient myocardial ischemia induced by coronary vasospasm at the distal LAD which perfuses a relatively wide area.     

Electrocardiographic observations of pure septal infarction: a case report]

We report a very rare case of pure septal infarction, which was closely examined with detailed electrocardiography (ECG). The patient is a 65-year-old man, who underwent percutaneous transluminal coronary angioplasty (PTCA) for exercise-induced angina. During PTCA for the target lesions in the left anterior descending artery (LAD) and diagonal branch, a large septal branch originating from the LAD was accidentally and completely occluded. Septal Q waves then disappeared from leads I, V5 and V6, and ST segments were elevated in leads V1 to V3, with concomitant ST depressions in leads I, II, aVF, V5 and V6. It was speculated that the initial electrical potential derived from the central septum may have been lost due to septal infarction, resulting in the disappearance of the septal Q waves. The present case disclosed the role of the interventricular septum in the genesis of septal Q waves in the left precordial leads.     

Clinical and hemodynamic aspects of single vessel coronary artery disease

Two-hundred consecutive patients with arteriosclerotic heart disease underwent complete clinical and hemodynamic evaluation. Fifty-two patients (26 per cent) had significant single vessel coronary artery disease and were compared to 148 patients with more extensive coronary artery disease and to a group of 14 normal patients. The single vessel disease group, when compared to the diffuse disease group, was characterized by a shorter duration of angina pectoris, lower frequency of a history of congestive heart failure or cardiomegaly, and a lower frequency of electrocardiographic (ECG) evidence of a transmural myocardial infarction. The combination of angina pectoris for three or more years with cardiomegaly was the only factor which completely separated the two coronary disease groups. Cardiomegaly, when present in single vessel involvement, was always due to left anterior descending (LAD) disease, together with an anterior infarction on ECG and left ventricular asynergy. The single vessel disease group included 32 patients with LAD disease, 17 with RCA, and 3 with circumflex artery involvement. Resting hemodynamics in these 52 patients (other than a higher left ventricular end-diastolic pressure and wall stress) were not significantly different from hemodynamics in a normal group. Patients with diffuse disease were characterized by many hemodynamic alterations and by left ventricular (LV) asynergy, when compared to the single vessel disease or normal groups. The diffuse disease group had a lower ejection fraction (EF) and an increased frequency of LV asynergy and coronary collateral circulation than did the LAD group. In the single vessel disease group LV asynergy did not correlate with the ECG. LV synergy, however, was not found in any patient in the LAD group with abnormal Q waves on ECG. The single vessel disease group included only five patients with increased end-diastolic volume (EDV) and all had LAD involvement, increased LV end-diastolic pressure, and decreased EF. The remaining 47 patients with normal LV-EDV revealed that the LAD group had abnormal pressure-volume relationships, indicating a decreased compliance of the left ventricle.     

Apical segmental dysfunction in hypertrophic cardiomyopathy: subgroup with unique clinical features

A segmental wall motion abnormality is an unusual finding in patients with hypertrophic cardiomyopathy. To clarify its clinical significance, 48 patients with hypertrophic cardiomyopathy were analyzed. Eight patients (Group A) had apical segmental dysfunction; 40 (Group B) had normal wall motion. No patient in either group had coronary artery stenosis on selective coronary arteriography. In all patients in Group A, apical segmental dysfunction was revealed by left ventriculography; however, it could be detected by echocardiography in only two patients in Group A. Left ventricular hypertrophy by electrocardiogram (ECG) was more common in Group B (p less than 0.05). Abnormal Q waves were more frequently discovered in Group A (p less than 0.005) and were recognized predominantly in the lateral leads. On serial ECGs, a gradual development of abnormal Q waves was noted in six of eight patients in Group A. Malignant arrhythmias were more common in Group A (p less than 0.001). In two patients in Group A, left ventricular dilation and congestive heart failure developed during the follow-up period. Thus, the presence of a Q wave in the lateral leads on an ECG in patients with hypertrophic cardiomyopathy may indicate the presence of apical segmental dysfunction. Left ventriculography should be performed to examine the presence of this abnormality and 24 h ambulatory ECG monitoring should be done to detect malignant arrhythmias in patients who have abnormal Q waves in the lateral leads. Patients with this unique type of hypertrophic cardiomyopathy need careful follow-up evaluation.     

Association between intraventricular myocardial systolic dyssynchrony and ventricular arrhythmias in patients with hypertrophic cardiomyopathy

BACKGROUND: The distribution and magnitude of left ventricular (LV) hypertrophy are not uniform in patients with hypertrophic cardiomyopathy (HCM), which results in regional heterogeneity of LV systolic and diastolic function. The aim of the study was to evaluate LV regional systolic asynchrony in patients with HCM by pulsed Doppler myocardial imaging (DMI). METHODS: We studied 35 HCM patients and 45 age- and sex-matched controls. By the use of DMI, the following five different basal myocardial segments were measured: systolic peak velocity (Sm); early- and late-diastolic peak velocities; pre-contraction time (Q-Sm) (from the beginning of Q-wave of ECG to the onset of Sm); intraventricular systolic delay (IntraV-Del) (difference of Q-Sm in different LV myocardial segments); interventricular delay (InterV-Del) (difference of Q-Sm between the most delayed LV segment and right ventricular lateral wall). RESULTS: DMI analysis showed in HCM lower myocardial systolic and early-diastolic peak velocities of all the analyzed segments. As for time intervals, controls showed homogeneous systolic activation of the ventricular walls. Conversely, HCM group, despite the absence of intraventricular conduction defects by surface ECG, showed significant both Inter- and IntraV-Del (P < 0.0001). Linear regression models pointed out independent positive associations of IntraV-Del with LV outflow gradient and septal wall thickness in HCM (P < 0.001). An IntraV-Del >30 msec well differentiated controls and HCM. In addition, an IntraV-Del > 45 msec (ROC curve) identified a subgroup of HCM patients with nonsustained ventricular tachycardia during Holter monitoring (90.9% sensitivity and 95.8% specificity). CONCLUSIONS: The impairment of intrarventricular systolic synchronicity is strongly related to increased septal thickness and LV outflow-tract gradient in HCM. DMI analysis may be able to select subgroups of HCM patients at an increased risk of ventricular tachyarrhythmias.     

Clinicopathologic study of abnormal Q waves in Kawasaki disease (mucocutaneous lymph node syndrome): An infantile cardiac disease with myocarditis and myocardial infarction

A correlative study of abnormal Q waves and pathologic findings was performed on 15 hearts from children with Kawasaki disease. Gross pathologic study revealed acute angiitis with pericarditis, acute myocarditis and coronary heart disease as the result of angiitis.Three hearts in infants with abnormal Q waves in leads I and aVL and chest leads had gross transmural fibrosis in the anteroseptal-lateral walls of the left ventricle. Coagulation necrosis (acute myocardial infarction) or fibrosis, or both, in more than 30 percent of the wall thickness in the posterior ventricular wall was found in four of five hearts in infants with abnormal Q waves in leads II, III and aVF. Seven of the 15 infants had no abnormal Q waves, and only 2 of the 7 had myocardial damage in over 30 percent of the wall thickness.In 9 of the 15 hearts there were 11 gross areas of fibrosis; in these hearts there was a corresponding severe stenosis of more than 90 percent due to organization in the major coronary arteries supplying these areas. In three hearts with coagulation necrosis, the coronary occlusion was caused by fresh large thrombi. In the six hearts without sizable fibrosis, the grade of stenosis due to organization was less than 75 percent in each of the major coronary arteries.Coronary aneurysm due to angiitis was seen in 12 of the 15 hearts, and at autopsy fresh large thrombi were seen in each aneurysm. Ten of the 12 hearts exhibited sizable areas of myocardial damage. Three hearts without aneurysm manifested angiitis with mild stenosis of less than 25 percent, but there were no macroscopic fresh thrombi in any of the major coronary arteries.Thus, abnormal Q waves in children with Kawasaki disease almost always reflect myocardial damage in over 30 percent of the wall thickness of the left ventricle. Electrocardiograms are useful to determine the anterior or posterior localization of the damage. Nevertheless, the possibility of transmural and nontransmural areas of damage cannot be excluded in the absence of abnormal Q waves.     

Usefulness of ST-segment elevation in the inferior leads in predicting ventricular septal rupture in patients with anterior wall acute myocardial infarction

The ventricular septum receives its blood supply from the septal perforators of the left anterior descending (LAD) coronary artery and the right coronary artery. However, when the LAD artery extends to the inferior wall, beyond the apex (so-called wrapped LAD), the ventricular septum near the apex receives blood supply only from the LAD artery. As a consequence, ventricular septal rupture (VSR) would seem more likely in myocardial infarction with occlusion of this type of LAD artery. To test this hypothesis, we compared electrocardiographic findings in 21 patients who had anterior acute myocardial infarction that was complicated by VSR with those in 275 patients who had acute myocardial infarction that was not complicated by VSR. We observed ST-segment elevation in all inferior leads (II, III, and aVF) in addition to anterior leads in 42.9% of patients (9 of 21) who had VSR but in only 3.6% of those (10 of 275) who did not have VSR. Abnormal Q waves appeared in all 3 inferior leads in 44.4% of patients (8 of 18) who had VSR but in only 4.0% of those (10 of 250) who did not have VSR. Thus, the incidence of ST-segment elevation and abnormal Q waves in the inferior leads was significantly (p <0.001) greater in the VSR group. In addition, multivariate analysis of patient characteristics, including advanced age, female gender, and coronary morphology, showed VSR to be significantly correlated with ST-segment elevation (odds ratio 16.93, 95% confidence interval 4.13 to 69.30) and abnormal Q waves (odds ratio 13.64, 95% confidence interval 3.16 to 58.79) in the 3 inferior leads. In conclusion, these electrocardiographic findings can be useful predictors of complication by VSR.     

Serial changes in left ventricular configuration and function in hypertrophic cardiomyopathy

Fifteen patients, 12 males and three females, with hypertrophic cardiomyopathy (HCM) including three of obstructive type (HOCM) were investigated to observe the long-term course of HCM. Left ventriculography and bi-ventriculography were performed twice serially in all cases. We studied the correlations between the serial ECG changes, especially the negative T wave, and the left ventricular configuration, wall thickness, and left ventricular function. Serial ECG changes included: 1) negativity of the T wave which developed or increased concomitantly with increased voltages of SV1 + RV5 (A-1 group: five cases), 2) the negativity decreased or resolved with decreased voltages of SV1 + RV5 (A-2 group: four cases), and 3) insignificant changes of both T waves and SV1 + RV5 (B group: six cases). In the right oblique views at end-diastole, the configuration of the left ventricle was classified in three forms; (1) spade form (S), (2) round form (R), and (3) intermediate form (SR). The results were as follows: 1. The A-1 group showed increased thickness of the apical and anterior walls, but the thickness of the posterior wall and interventricular septal wall did not change serially. In three cases, the thickness of the interventricular septum showed mild hypertrophy at the initial and final observations. The configuration changed from the R or SR form to the S form. Diastolic dysfunction (peak dV/dt/V, peak dV/dt/EDV) was progressive, but end-diastolic volume and ejection fraction did not change. 2. The A-2 group showed the significantly decreased thickness of the apical and anterior walls. The thicknesses of the posterior wall and interventricular septal wall tended to decrease in all cases. In three cases (75%), the interventricular septal wall was markedly hypertrophied on the initial observation. The configuration changed from the S or SR form to the R form. Left ventricular diastolic function and ejection fraction decreased significantly and end-diastolic volume increased. Two cases showed clinical pictures of dilated cardiomyopathy at the final observation. 3. In the B group, there were no marked changes in wall thickness, left ventricular configuration, or systolic and diastolic functions. In conclusion, serial changes in left ventricular configuration, wall thickness, especially of the anterior and apical walls, and left ventricular function were all compatible with the serial changes of the ECG in hypertrophic cardiomyopathy.(ABSTRACT TRUNCATED AT 400 WORDS)     

ECG pattern of left ventricular hypertrophy in nonobstructive hypertrophic cardiomyopathy: the significance of the mid-precordial changes.

A review of electrocardiograms from 33 patients with nonobstructive hypertrophic cardiomyopathy was made. In 22 patients there was noted a high QRS voltage, depression of the ST segment, and inversion of the T wave, satisfying the diagnostic criteria of left ventricular hypertrophy with the abnormal changes not only extending to the midprecordial leads but showing the most striking abnormal changes in Lead V4 in 20 patients. The frontal plane electrical axis was normal (around 60 degrees), with the most remarkable changes in Lead II. In the VCG, the magnitude of the QRS loop was increased and directed anteriorly and to the left, and the T loop was deviated posteriorly and to the right opposite the QRS loop. The asymmetric septal and apical hypertrophy was noted on echocardiography and/or angiocardiography. The coronary arteries were normal without significant obstruction in selective coronary angiography. It was postulated that the asymmetric septal and apical hypertrophy was reflected in this ECG pattern. The recognition of this ECG pattern provides pertinent information in the clinical detection of nonobstructive HCM.     

Disappearance of septal q-wave or appearance of abnormal Q-wave in V5 and V6 after onset of anterior acute myocardial infarction: electrocardiographic and angiographic correlations

Background The factors influencing the q-wave changes in V5 and V6 during anterior acute myocardial infarction (AMI) have not been thoroughly described. Methods We studied 70 patients with a first anterior AMI, in whom the electrocardiogram (ECG) showed either disappearance of the normal septal q wave (n = 24) or presence of pathological Q wave in V5 and V6 (n = 46) during follow-up. The ECG and coronary angiography findings were correlated. Results There was no difference between the 2 groups in the culprit site proximal to S1 (46% vs. 36%, P = 0.405), but the culprit site was more frequently located proximal to D1 in the group with abnormal Q wave (21% vs. 67%, P = 0.001). Patients with disappearance of the septal q wave more often had a large obtuse marginal branch (46 % vs. 22%, P = 0.037) and disappearance of the r wave in V1 (88% vs. 7%, P = 0.001). Patients with abnormal Q-wave more often had a large LAD (42% vs. 71%), small r wave or tall or wide R wave in V1 (0 % vs. 89 %, P = 0.001) and abnormal Q waves in the inferior leads (33% vs. 59%, P = 0.044). Conclusions In patients with first anterior AMI, q wave changes in V5 and V6 correlated with the morphology in V1 . Emerging abnormal Q wave in V5 / V6 predicted the culprit lesion in a large LAD proximal to D1 , but disappearance of the septal q wave could not predict the culprit lesion proximal to S1 .