Angled interventricular septum on echocardiography: Anatomic anomaly or technical artifact?

An acutely angled interventricular septum has been reported to constitute a distinct two-dimensional echocardiographic geometric pattern that may permit a false M-mode echocardiographic recording of asymmetric septal hypertrophy. In light of experience suggesting that the angle between the aortic root and interventricular septum varied with the intercostal space of the transducer, 45 subjects were prospectively studied by two-dimensional and M-mode echocardiography. Parasternal long- and short-axis views were obtained from two to four intercostal spaces in each subject. Two-dimensional echographic cursor-generated M-mode echocardiograms were obtained from the long-axis views; interventricular septal and left ventricular posterior wall thickness was measured from both the two-dimensional and M-mode echocardiograms. On two-dimensional echocardiography, the angle between the aortic root and septum became more acute as a progressively lower intercostal space was used (p less than 0.001). Although no change in septal thickness was apparent, the septal thickness significantly increased as a progressively lower intercostal space was used. On M-mode echocardiography, 21 subjects (47%) demonstrated asymmetric septal hypertrophy (septal/posterior wall thickness ratio greater than 1.3) from at least one intercostal space, but this was confirmed by the two-dimensional technique in only 4 subjects (9%). Thus, a two-dimensional echocardiographic recording of an angled interventricular septum can be produced by positioning the transducer in a low intercostal space, and caution must be used in the interpretation of asymmetric septal hypertrophy on M-mode echocardiograms. Two-dimensional echocardiography is a useful means of identifying subjects with apparent asymmetric septal hypertrophy that often may be the result of a technical artifact.     

Limitation of angiography to identify the culprit plaque in acute myocardial infarction with coronary total occlusion utility of coronary plaque temperature measurement to identify the culprit plaque.

OBJECTIVES: The purpose of this study was to test the hypothesis that the maximal temperature (Tmax) site, as measured by thermal wire, coincides with the culprit plaque by intravascular ultrasound (IVUS) in patients with acute myocardial infarction (AMI). BACKGROUND: Subsequent thrombosis developing to the proximal region from the site of plaque rupture or erosion can potentially complicate the ability of coronary angiography to identify the accurate culprit plaque in patients with coronary total occlusion. METHODS: In 45 consecutive patients with a first anterior AMI, the Tmax site by thermal wire and the culprit plaque by IVUS were evaluated in the left anterior descending coronary artery (LAD). RESULTS: Twenty-five patients had LAD total occlusion, and the remaining 20 had LAD reperfusion. In both groups of patients, the Tmax site was significantly more distal to the angiographically most stenotic site or occlusive site (reperfusion: mean distance [MD] = 1.1 mm distal, 95% confidence interval [CI] 0.3 to 1.9 mm, p = 0.01; total occlusion: MD = 8.8 mm distal, 95% CI 8.0 to 9.6 mm, p < 0.0001). The culprit plaques by IVUS approximately coincided with those by angiography or thermal wire in patients with reperfusion. However, the angiographic occlusive site was significantly more proximal to the culprit plaque by IVUS (MD = 9.2 mm, 95% CI 7.9 to 10.6 mm, p < 0.0001), but the Tmax site coincided with the culprit plaque by IVUS (MD = 0.3 mm distal, 95% CI 0.3 mm proximal to 1.0 mm distal, p = 0.293) in patients with total occlusion. CONCLUSIONS: Temperature measurement of coronary plaque enables accurate localization of the culprit plaque in AMI with coronary total occlusion.     

Effects of glucose abnormalities on in-hospital outcome after coronary intervention for acute myocardial infarction.

BACKGROUND: The effects of glucose abnormalities on outcomes after percutaneous coronary intervention (PCI) remain unclear. We examined the association between glucose abnormalities and in-hospital outcome in patients undergoing PCI for acute myocardial infarction (AMI). METHODS AND RESULTS: A total of 849 patients with AMI who were admitted within 12 h after symptom onset and underwent emergency PCI were classified according to the presence or absence of admission hyperglycemia, defined as a blood glucose level on admission of >11 mmol/L and whether they had a history of diabetes mellitus: group 1 (n = 504), non-diabetic patients without admission hyperglycemia; group 2 (n = 111), diabetic patients without admission hyperglycemia; group 3 (n = 87), non-diabetic patients with admission hyperglycemia; and group 4 (n = 147), diabetic patients with admission hyperglycemia. Among groups 1, 2, 3 and 4, in-hospital mortality was 2.6, 2.7, 11.5 and 8.8%, respectively (p < 0.01). Multivariate analysis showed that compared with group 1 patients, the odds ratio (95%confidence interval) for in-hospital mortality among those in groups 2, 3, and 4 were 0.80 (0.24-2.60, p = 0.708), 2.29 (1.10-5.49, p = 0.039), and 2.14 (1.14-4.69, p = 0.048), respectively. CONCLUSIONS: In-patients undergoing PCI for AMI, admission hyperglycemia, irrespective of the presence or absence of diabetes, is associated with increased in-hospital mortality, whereas diabetes without admission hyperglycemia is not.     

Monophasic transmitral flow pattern with less increase in heart rate indicates left ventricular dysfunction.

When heart rate (HR) increases, mitral flow can become monophasic. Prolonged isovolumic contraction and relaxation time (ICT and IRT), directly related to left ventricular (LV) function, can potentially influence the HR with monophasic mitral flow. The present study investigated the relation between HR that causes monophasic flow and LV function. During diagnostic catheterization, HR was increased using right atrial pacing by 2 beats/min every 2 min in a stepwise manner until the development of monophasic mitral flow in 17 patients with normal sinus rhythm. ICT, IRT, end-diastolic and end-systolic LV volumes, LV ejection fraction, LV peak + and -dP/dt, peak (+dP/dt)/P, and the relaxation time constant (tau) were measured by Doppler echocardiography or catheterization when monophasic mitral flow developed. The monophasic HR varied from 74 to 106 beats/min. By univariate analysis, ICT (p<0.01, r2=0.73), LV peak +dP/dt (p<0.05, r2=0.37), peak (+dP/dt)/P (p<0.01, r2=0.71), peak -dP/dt (p<0.05, r2=0.25), and tau (p<0.05, r2=0.33) had a significant correlation with monophasic HR. By multivariate analysis, prolonged ICT and reduced LV peak -dP/dt independently contributed to monophasic mitral flow with less increase in HR. Monophasic mitral flow with less increase in HR indicates impaired LV systolic and diastolic function during isovolumic contraction and relaxation.     

Dystrophin-deficient myocardium is vulnerable to pressure overload in vivo

OBJECTIVE: Dystrophin provides mechanical reinforcement to the membranes of myocytes. Dystrophin abnormalities are known to cause cardiomyopathy and skeletal muscle disorders; however, the pathogenesis of these abnormalities remains unclear. Dystrophin-deficient skeletal muscle is vulnerable to stresses such as stretch and hypo-osmotic shock. We investigated whether the myocardium of dystrophin-deficient (mdx) mice shows increased vulnerability to acute pressure overload in vivo. METHODS AND RESULTS: Abdominal aortic banding was performed in 12-week-old mdx and control mice. The aortic pressure was measured by cannulation of the right carotid artery at the time of sacrifice. Systolic pressures in mdx mice at 0, 1, 2, 7 and 14 days after aortic banding were 100 +/- 11, 119 +/- 7, 123 +/- 4, 134 +/- 11 and 130 +/- 10 mmHg, respectively. Microscopic analysis revealed focal lesions in the left ventricular wall in banded mdx mice. These lesions consisted of damaged myocytes and inflammatory cells, and also of fibrosis at a late stage. Similar lesions were not observed in non-banded or banded control mice. The proportion of areas of lesions to total left ventricular area increased over time: 1.0 +/- 0.6% in mdx mice without aortic banding (sham, n = 6), and 1.7+/-1.4% 1 day (n = 6, vs. sham, NS), 2.6 +/- 1.9% 2 days (n = 7, vs. sham, P < 0.05), 6.3+ /- 6.5% 7 days (n = 13, vs. sham, P < 0.05) and 9.9 +/- 8.3% 14 days after aortic banding (n=15, vs. sham, P < 0.01). Furthermore, linear regression analysis revealed a significant correlation between percentage of lesion area and systolic pressure in mdx mice (P < 0.05). CONCLUSION: Dystrophin-deficient myocardium is more vulnerable than normal myocardium to pressure overload in vivo. This result has two clinical implications: (1) the patients with dystrophynopathy, such as the Duchenne and the Becker types of muscular dystrophy and X-linked type of dilated cardiomyopathy, who develop arterial hypertension should be treated aggressively, and (2) they should avoid stresses that elevate blood pressure.     

Mitral valve prolapse in short-term experimental coronary occlusion: a possible mechanism of ischemic mitral regurgitation

Experimental coronary occlusions were carried out in 12 closed-chest dogs to investigate the functional anatomic characteristics of the mitral valve complex during acute myocardial ischemia. Two-dimensional echocardiography was used to assess left ventricular function, the mitral valve complex, and left atrial size. Presence of mitral regurgitation was assessed by left ventricular contrast echocardiography. Thirty-seven coronary occlusions of up to 10 min in duration were carried out in proximal or distal locations in the left anterior descending and the left circumflex coronary arteries. Mitral regurgitation, which was mild in severity as judged by a small rise in pulmonary artery wedge pressures, was observed in 15 of 37 brief coronary occlusion experiments. Mitral valve prolapse was noted in all 15 experiments, as well as in four additional studies in which mitral regurgitation was not seen. The development of experimental mitral valve prolapse was explained by measurements that demonstrated a relative displacement of the papillary muscle tips toward the mitral orifice. We conclude that mitral valve prolapse is a common sequela of short-term coronary occlusion and is often associated with mild mitral regurgitation. Relative displacement of ischemic papillary muscles toward the mitral orifice appears to be a likely mechanism of acute ischemic mitral valve prolapse.     

Osteochondral autograft transplantation for juvenile osteochondritis dissecans of the knee: a series of twelve cases

Purpose

The purpose of this study was to evaluate the clinical outcomes of osteochondral autograft transplantation (OAT) for juvenile osteochondritis dissecans (JOCD) lesions of the knee, especially time to return to sports.

Methods

Twelve knee JOCD lesions with OCD grade 3 and 4 categorised by magnetic resonance imaging (MRI) were treated with OAT. Nine male and two female skeletally immature patients averaging 13.7 years old were included. The OCD lesions were assessed arthroscopically and then fixed in situ using multiple osteochondral plugs harvested under fluoroscopy from the distal femoral condyle without damaging the physis. International Cartilage Repair Society (ICRS) score and Lysholm score were assessed pre- and postoperatively.

Results

After a mean follow-up of 26.2 ± 15.1 months, the International Knee Documentation Committee (IKDC) subjective score significantly improved (p < 0.01). According to the IKDC score, objective assessment showed that ten of 12 (83 %) had excellent results (score: A) after OAT and significantly improved (p < 0.01). Based on ICRS criteria, results were satisfactory in all patients. No patients experienced complications at the graft harvest site. All patients returned to their previous level of athletic activity at an average of 5.7 months after the surgery.

Conclusions

OAT for JOCD of the knee provided satisfactory results in all patients at a mean follow-up of 26.2 months.     

Diastolic pulmonary forward flow associated with pulmonary regurgitation demonstrated by Doppler echocardiography

To demonstrate diastolic pulmonary forward flow, pulsed and continuous wave Doppler echocardiograms were recorded in four patients with postoperative residual pulmonary stenosis and regurgitation (Group I). To clarify the mechanism, we further examined 24 patients with pulmonary regurgitation without diastolic pulmonary forward flow, including three patients with surgical correction of tetralogy of Fallot (Group IIa) and 21 patients with functional pulmonary regurgitation (Group IIb), and compared the peak velocity and pressure half time of pulmonary regurgitation among the three groups. Diastolic pulmonary forward flow was characterized as a flow signal which began after the abrupt cessation of pulmonary regurgitation and continued until the beginning of ejection flow. The onset of the flow coincided with that of premature opening of the pulmonary valve, and was following atrial contraction in one, before atrial contraction in two, and mid-diastolic in one. The velocity of diastolic pulmonary forward flow was increased during inspiration and its maximum velocity was 1.3 m/sec. Simultaneous recording of pressures and continuous wave Doppler echo performed in two patients in Group I showed the equalization of right ventricular and pulmonary artery pressures during the flow. There was no significant difference in the peak velocity of pulmonary regurgitation among the three groups of patients. The mean pressure half time was significantly shortened in patients in Group I (90 +/- 11 msec) compared with those in patients in Group IIa (143 +/- 40 msec, p less than 0.05) and Group IIb (310 +/- 71 msec, p less than 0.001). In conclusion, a diastolic pulmonary forward flow seems to be produced by the rapid equalization of right ventricular and pulmonary artery pressures due to severe pulmonary regurgitation in the face of decreased right ventricular compliance.