Anatomy of the human atrioventricular junctions revisited.
(41/768)
There have been suggestions made recently that our understanding of the atrioventricular junctions of the heart is less than adequate, with claims for several new findings concerning the arrangement of the ordinary working myocardium and the specialised pathways for atrioventricular conduction. In reality, these claims are grossly exaggerated. The structure and architecture of the pathways for conduction between the atrial and ventricular myocardium are exactly as described by Tawara nearly 100 years ago. The recent claims stem from a failure to assess histological findings in the light of criterions established by Monckeberg and Aschoff following a similar controversy in 1910. The atrioventricular junctions are the areas where the atrial myocardium inserts into, and is separated from, the base of the ventricular mass, apart from at the site of penetration of the specialised axis for atrioventricular conduction. There are two such junctions in the normal heart, surrounding the orifices of the mitral and tricuspid valves. The true septal area between the junctions is of very limited extent, being formed by the membranous septum. Posterior and inferior to this septal area, the atrial myocardium overlies the crest of the ventricular septum, with the atrial component being demarcated by the landmarks of the triangle of Koch. The adjacent structures, and in particular the so-called inferior pyramidal space, were accurately described by McAlpine (Heart and Coronary Arteries, 1975). Thus, again there is no need for revision of our understanding. The key to unravelling much of the alleged controversy is the recognition that, as indicated by Tawara, the atrioventricular node becomes the atrioventricular bundle at the point where the overall axis for conduction penetrates into the central fibrous body. There are also marked differences in arrangement, also described by Tawara, between the disposition of the conduction axis in man as compared to the dog. (+info)
OBJECTIVE: The objective of this study is to evaluate the one-year outcome of the first 50 patients who underwent nonsurgical septal reduction for symptomatic hypertrophic obstructive cardiomyopathy at our institution. BACKGROUND: Left ventricular outflow tract obstruction is an important determinant of clinical symptoms in patients with hypertrophic obstructive cardiomyopathy. Nonsurgical septal reduction is a new therapy that has been shown to result in left ventricular outflow tract gradient reduction and resolution of symptoms immediately after the procedure and on midterm follow-up. METHODS: Fifty patients with hypertrophic obstructive cardiomyopathy who underwent nonsurgical septal reduction at our institution and completed 1-year follow-up are described. Complete history, physical examination, two-dimensional echocardiography with Doppler and exercise treadmill testing have been analyzed. RESULTS: The mean age of the study group was 53 +/- 17 years. All patients had refractory symptoms before enrollment. Ninety-four percent had class III or IV New York Heart Association class symptoms at baseline compared to none at 1 year (p < 0.001). The exercise duration increased by 136 s at 1 year (p < 0.021). Only 20% of patients were either receiving beta-blockers or calcium-channel blockers on follow-up. The resting left ventricular outflow tract gradient decreased from 74 +/- 23 mm Hg to 6 +/- 18 mm Hg (p < 0.01) and from 84 +/- 28 mm Hg to 30 +/- 33 mm Hg (p < 0.01) in patients with dobutamine-provoked gradient at one year. These changes are associated with decreased septal thickness and preserved systolic function. CONCLUSION: Nonsurgical septal reduction therapy is an effective therapy for symptomatic patients with hypertrophic obstructive cardiomyopathy with persistence of the favorable outcome up to one year after the procedure. (+info)
Prolongation of QT interval and ventricular septal hypertrophy.
(43/768)
Long QT syndrome (LQTS) is a prime example of interplay between molecular biology, cellular physiology, and organ physiology. Both the congenital and acquired forms of LQTS are due to intrinsic and/or acquired abnormalities of the ionic currents responsible for cardiac repolarization. We analyzed the QTc interval, QRS axes and interventricular septal thickness (IVST) in 41 patients who had a prolonged QT interval on routine electrocardiography (ECG) (5 females and 36 males, mean age 65+/-13 years). The QRS axis of patients in the LQTS group (27+/-49 degrees) was significantly lower (p < 0.05) than in the control group (46+/-26 degrees). However, the IVST in the LQTS group (10+/-2 mm) was significantly thicker than in the control group (9+/-1 mm) (p < 0.05), while the WTd was not significantly different. The QTc interval in patients with ventricular septal hypertrophy (IVST > or = 12 min, 478.8+/-7.9 msec) was significantly longer (p < 0.05) than in the normal group (IVST < 12 mm, 472.1+/-17.5 msec). In conclusion, the results of this preliminary study suggest that prolongation of the QT interval on ECG should prompt screening for electrocardiographic evidence of ventricular hypertrophy in patients with this disease. (+info)
Coronary stent implantation in a septal perforator artery: case report and review of the literature.
(44/768)
Septal perforator arteries play an important role in the blood supply of the anterior interventricular septum. Their intramyocardial course makes them inaccessible for coronary bypass revascularization. Although modern catheter-based techniques might be superior to coronary bypass grafting in offering the most complete revascularization in selected patient populations, a systematic review of the literature revealed a paucity of data regarding the outcome of these patients. The present report describes coronary stent implantation in a dominant septal perforator artery and the analysis of the anatomic relationship between the stent and the intraventricular septum using a new imaging technique, catheter-based intracardiac ultrasound. (+info)
Improvement in midwall myocardial shortening with regression of left ventricular hypertrophy.
(45/768)
Despite normal indices of left ventricular (LV) chamber function, patients with LV hypertrophy (LVH) due to hypertension are thought to have depressed midwall systolic shortening compared with normotensives. The aims of the present study were (1) to confirm this observation and (2) to assess the effects of antihypertensive therapy that cause regression of LVH on LV systolic function assessed at both the midwall and endocardium. Thirty-eight previously untreated hypertensive subjects with LVH underwent echocardiography and were compared with 38 normotensive control subjects. Comparisons between the group with LVH and the control group revealed no significant differences in cardiac output (4. 32+/-0.23 versus 4.55+/-0.21 L/min), ejection fraction (62.5+/-2% versus 66.4+/-1.07%), or endocardial fractional shortening (34.5+/-1.45% versus 37.0+/-0.82%), but shortening assessed at the midwall was significantly less in the group with LVH (17.9+/-1.11% versus 21.6+/-0.63%, P<0.01). Subsequently, 32 patients with uncontrolled hypertension (24 previously untreated and 8 on existing antihypertensive therapy) underwent treatment with ramipril, with the addition of felodipine and bendrofluazide if required, to reduce blood pressure to <140/90 mm Hg. These 32 patients underwent echocardiography at baseline, after blood pressure control, and after an additional 6 months of tight blood pressure control. Good blood pressure control was achieved after 6 months compared with baseline (143/86+/-2.8/1.4 versus 174/103+/-4.1/1.9 mm Hg; P<0.01) with significant regression of LV mass index (124+/-3.4 versus 145+/-3.8 g/m(2), P<0.01). LV fractional shortening assessed at the midwall improved with regression of LVH (21.9+/-0.84 and 18.7+/-1. 19%, P<0.05), with posttreatment midwall shortening being similar to that of the normal control subjects evaluated in the first study. Hypertensive patients with LVH have depressed midwall systolic shortening despite normal indices of LV chamber function. Regression of LVH after good blood pressure control improved midwall shortening to normal levels. (+info)
Reduction of atrial defibrillation threshold with an interatrial septal electrode.
(46/768)
BACKGROUND: The standard lead configuration for internal atrial defibrillation consists of a shock between electrodes in the right atrial appendage (RAA) and coronary sinus (CS). We tested the hypothesis that the atrial defibrillation threshold (ADFT) of this RAA-->CS configuration would be lowered with use of an additional electrode at the atrial septum (SP). METHODS AND RESULTS: Sustained atrial fibrillation was induced in 8 closed-chest sheep with burst pacing and continuous pericardial infusion of acetyl-ss-methylcholine. Defibrillation electrodes were situated in the RAA, CS, pulmonary artery (PA), low right atrium (LRA), and across the SP. ADFTs of RAA-->CS and 4 other lead configurations were determined in random order by use of a multiple-reversal protocol. Biphasic waveforms of 3/1-ms duration were used for all single and sequential shocks. The ADFT delivered energies for the single-shock configurations were 1.27+/-0.67 J for RAA-->CS and 0. 86+/-0.59 J for RAA+CS-->SP; the ADFTs for the sequential-shock configurations were 0.39+/-0.18 J for RAA-->SP/CS-->SP, 1.16+/-0.72 J for CS-->SP/RAA-->SP, and 0.68+/-0.46 J for RAA-->CS/LRA-->PA. Except for CS-->SP/RAA-->SP versus RAA-->CS and RAA-->CS/LRA-->PA versus RAA+CS-->SP, the ADFT delivered energies of all of the configurations were significantly different from each other (P:<0. 05). CONCLUSIONS: The ADFT of the standard RAA-->CS configuration is markedly reduced with an additional electrode at the atrial SP. (+info)
Tonic regulation of vascular tone by nitric oxide and chloride ions in rat isolated small coronary arteries.
(47/768)
We have investigated the involvement of Cl(-) in regulating vascular tone in rat isolated coronary arteries mounted on a small vessel myograph. Mechanical removal of the endothelium or inhibition of nitric oxide (NO) synthase with N(omega)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) led to contraction of rat coronary arteries, and these contractions were sensitive to nicardipine (10(-6) M). This suggests that release of NO tonically inhibits a contractile mechanism that involves voltage-dependent Ca(2+) channels. In arteries contracted with L-NAME, switching the bathing solution to physiological saline solution with a reduced Cl(-) concentration potentiated the contraction. DIDS (5 x 10(-6)-3 x 10(-4) M) caused relaxation of L-NAME-induced tension (IC(50) = 55 +/- 10 microM), providing evidence for a role of Cl(-). SITS (10(-5)-5 x 10(-4) M) did not affect L-NAME-induced tension, suggesting that DIDS is not acting by inhibition of anion exchange. Mechanical removal of the endothelium led to contraction of arteries, which was sensitive to DIDS (IC(50) = 50 +/- 8 microM) and was not affected by SITS. This study suggests that, in rat coronary arteries, NO tonically suppresses a contractile mechanism that involves a Cl(-) conductance. (+info)
Echoventriculographic detection, localization, and quantification of left ventricular asynergy in acute myocardial infarction. A correlative echo- and electrocardiographic study.
(48/768)
"Echoventriculography", an echocardiographic method specially developed to scan the regional function of the left ventricle, is introduced for studying left ventricular wall motion alteration in patients with acute myocardial infarction. Purposeful probe directions, a 2:1 magnification, and careful adjustment of the gain and reject levels allowed a direct echocardiographic scanning of practically the entire left ventricle. Technically acceptable echoventriculograms were obtained from the upper and lower halves of the septal, anterior, lateral, and postero-inferior left ventricle segments in all observations on 30 consecutive patients with acute myocardial infarction. Various degrees of regional left ventricular asynergy were present in 100 per cent of the patients with acute myocardial infarction. In contrast, synergic ventricular segmental wall motion was observed in 40 healthy subjects. Pronounced asynergy was already detectable within 12 hours from onset of the symptoms of acute myocardial infarction. Echoventriculography detected acute left ventricular asynergy as well in the anteroseptal or lateral as in the posteroinferior locations. The anterior and/or septal infarction (13 of the 30 patientsy always showed a paradoxical systolic motion of the, generally large, infarcted areas. The amplitude of abnormal outward motion was up to 5 mm. In the posteroinferior infarctions (17 patients) akinetic or hypokinetic modes prevailed. The contractile function of the uninvolved segments could be measured at the same time. Hypercontractile left ventricular wall motion was common in these healthy areas in acute myocardial infarction. These findings provide useful insight into the various components of the overall left ventricular pump function in acute myocardial infarction. The validity of the echoventriculographic evaluations of the segmental left ventricular function subsets was further confirmed in 2 patients undergoing left ventricular cineangiographic studies and in 2 by necropsy. The site of the asynergic left ventricular wall motion abnormalities correlated excellently with electrocardiographic prediction of the site of acute myocardial infarction. The echoventriculographic analysis proved to be more accurate in detecting asynergy than was the electrocardiogram. This new echoventriculographic method may become a useful tool for serial noninvasive alalysis of left ventricular performance, in detecting both the asynergic areas and the reserve function of the normal regions in acute myocardial infarction. (+info)