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The commonest cause of breathlessness in hypertrophic cardiomyopathy (HCM) is left ventricular outflow tract (LVOT) obstruction which improves with its removal. However, in the absence of outflow tract obstruction, as in dilated cardiomyopathy, patients may be limited by similar symptoms, thus suggesting a potential common mechanism for the two conditions. We aimed to assess cardiac function at the time of symptoms in a group of unselected patients with HCM to identify other patterns of cardiac dysfunction which coincide with their breathlessness.We studied 37 HCM patients (aged 55 ± 15 years, 13 female) with septal thickness15 mm and 17 controls (aged 58 ± 12 years, 12 female) using Doppler echocardiography, at rest and at peak dobutamine stress. Stress end points were symptoms,20 mmHg drop in systolic blood pressure, arrhythmia, or maximum dobutamine dosage of 40 μg/kg/min.At rest: LV systolic function was maintained (EF 68 ± 7 v 76 ± 12%, respectively), LVOT velocity raised (p0.005), lateral and septal long axis amplitude reduced (p0.05 and p0.005, respectively) and dyssynchronous and QRS duration was also broader (p0.005) in patients compared to controls. At peak stress: Overall LVOT velocities were higher in patients than controls (4.3 ± 1.7 v 1.7 ± 1.0m/s, p0.005, respectively) due to systolic anterior movement of the mitral valve and mitral regurgitation developing. In the 15 patients who did not develop significant LVOT obstruction (velocity4m/s), LV ejection time increased and peak systolic amplitude did not increase. In the 10 patients with neither LVOT obstruction nor restrictive filling, QRS duration prolonged by 12 ms (p0.05), post-ejection shortening worsened and peak systolic amplitude fell (p0.005). Also, LV ejection time prolonged by 5s/min (p0.05), filling time failed to increase as it did in controls (p0.005) and Tei index was higher than controls (p0.01).Exertional breathlessness in HCM is associated with LV outflow tract obstruction and functional mitral regurgitation in almost two thirds of patients. The remaining one third have either resistant restrictive physiology or dyssynchronous cavity at fast heart rate. Despite similar exercise limiting breathlessness in the three groups, means of management should be quite different.

To evaluate the predictors for mortality following aortic valve replacement (AVR) in elderly patients with aortic stenosis (AS).112 consecutive elderly AS patients (aged 77+/-2 years) with AVR between 1998 and 2003 were studied. Clinical and echocardiographic data of LV function were recorded before and 46 months after AVR. Results were compared with 72 younger patients (aged 60+/-1 years). Outcome measures were 30-day and long-term all cause mortalities.Elderly patients had higher NYHA class, more frequent atrial fibrillation, coronary artery disease, emergency operation and use of bioprosthetic valves. They also had shorter E-wave deceleration time (DT) and larger left atria (p0.05 for all). 30-day mortality was 12% vs 4% (Log Rank x(2)=3.02, p=0.08) and long term mortality was 18% vs 7% (Log Rank x(2)=4.38, p=0.04) in two groups respectively. Age was not related to mortality after adjustment for other variables. Among all variables, anemia (OR 4.20, CI: 1.02-6.86, p=0.04), cardiopulmonary bypass (CPB) time (OR 1.02, CI 1.01-1.04, p0.01), significant prosthesis patient mismatch (PPM) (OR 5.43, CI 1.04-18.40, p0.05) were associated with 30-day mortality in elderly patients. Their long-term mortality was related to CBP time (OR 1.02, CI 1.00-1.05, p=0.04), PPM (OR 4.64, CI 1.33-16.11, p=0.02) and raised left atrial pressure: DT (OR 0.94, CI 0.84-0.99, p=0.03) and pulmonary arterial systolic pressure (OR 1.12, CI 1.03-1.19, p0.001).Peri-operative AVR survival is encouraging. While pre-operative anemia and a longer CBP time determine early mortality, long term mortality is related to PPM, LV diastolic dysfunction and secondary pulmonary hypertension.

BACKGROUND: The relationship between left ventricular (LV) long and short axes, aortic pressure (P), flow velocity (U) and wave intensity is not well established. METHODS: Eleven dogs were anaesthetized and mechanically ventilated and LV long and minor axes shortening velocities were calculated using ultrasound crystals. P and U were measured in the ascending aorta using a high fidelity pressure catheter and ultrasonic flow transducer. RESULTS: Pre-ejection: The LV minor axis began to shorten as the long axis lengthened creating LV shape change. Early ejection: The aortic valve opened 83+/-20 ms after the ECG Q-wave. Aortic P and U simultaneously increased; peak aortic velocity and maximum minor axis shortening velocity (M(max)) occurred at 152+24 and 147+24 ms, respectively; p=0.66, intra-class correlation ICC 0.93). M(max) also corresponded to the time when the reflected compression wave arrived back to the heart (ICC 0.75). Late ejection: LV long axis reached its peak shortening velocity 28+21 ms later than the minor axis at 175+/-33 ms, coinciding with peak LV pressure (187+25 ms; p=0.77, ICC 0.65) and onset of the forward expansion wave (177+28 ms, p=0.88, ICC 0.89). Both axes then continued to slow until 210+/-30 ms when an increased rate of decline of shortening velocity corresponded with peak aortic pressure. CONCLUSION: Long axis peak shortening velocity lagged consistently behind the minor axis, representing a degree of normal asynchrony. The arrival of the reflected wave appears to bring about the slowing down of the minor axis.

The search for optimal sedation for transesophageal echocardiography (TEE) continues. We hypothesized that the ultra-short acting opioid remifentanil combined with very low-dose midazolam would provide a better sedation and recovery profile compared to midazolam alone.41 consecutive outpatients scheduled for TEE received either IV midazolam (group M, 2.5 mg bolus plus 1 mg increments repeated as needed, n=18) or a combination of a low-dose IV bolus of midazolam (0.5 mg) plus an infusion of remifentanil (group RM, 0.1 mcg/kg/min, reduced to 0.08 mcg/kg/min after probe insertion, n=23). All patients received topical pharyngeal anesthesia with 2 puffs of lidocaine 4% spray. We recorded BP, SpO(2), HR, time-to-discharge (modified Aldrete score of 13), duration of procedure, resource utilization, complications, ease of probe introduction, ease and quality of the procedure. Patients' satisfaction with sedation was assessed using the Iowa Satisfaction with Anesthesia Scale (ISAS).Mean dose of midazolam in group M was 3.7+/-1.3 mg. Median time-to-discharge was significantly reduced in the RM group compared with the M group (5 (5-10) vs. 30 (5-240) min, p0.0001), with 22 of the 23 group RM patients ready for "street discharge" within 5 min of removal of the TEE probe. Ease of probe insertion (p=0.001), resource utilization (p=0.0001), patient satisfaction (p=0.03) and overall ease and quality of the procedure (p=0.0001) were significantly better in the RM group than in the M group. No episodes of desaturation were observed.This is the first report of the use of an ultra-short acting opioid, remifentanil, combined with a low-dose of midazolam, as a sedative technique for outpatient TEE. In this pilot, non-randomized prospective study, remifentanil plus low-dose midazolam provided better sedation than our current practice of higher bolus doses of midazolam alone. This novel approach is associated with improved procedure tolerance, faster recovery and minimal resource utilization. A randomized, controlled study is under way to verify our preliminary results.

We aimed to identify the most sensitive echocardiographic measurements that predict recovery of left ventricular function following valve replacement surgery in patients with severe aortic stenosis (AS) and LV dysfunction.We studied 66 patients (mean age 70+/-2 years, 53 male) who underwent AVR for severe AS with concurrent LV dysfunction between 1998 and 2003 at the Royal Brompton Hospital. Clinical symptoms, co-morbidities and echocardiographic measurements of LV function were recorded before and at a median follow-up of 46 months after AVR. Pre-operative LV systolic dysfunction was defined as LV ejection fraction (EF)50% and the post-op LV recovery as an increase of EF10%.Following AVR peak aortic pressure gradient decreased and aortic valve area index increased (64+/-3 to 19+/-1 mm Hg and 0.30+/-0.01 to 0.89+/-0.03 cm(2)/m(2), p0.001 for both). LV EF increased (from 45+/-1 to 54+/-2%; p0.001) and the LV dimensions fell (LVEDD index: from 33+/-1 to 30+/-1 mm/m(2); and LVESD index: from 27+/-1 to 20+/-1 mm/m(2); p0.01 for both). LV diastolic dysfunction improved as evidenced by the fall in E/A ratio (from 2.6+/-0.2 to 1.9+/-0.4) and prolongation of total filling time; (from 29.2+/-0.6 to 31.4+/-0.5 s/min, p=0.01 for both). Among all echocardiographic variables, LV dimensions (LVEDD index, OR 0.70, CI 0.52-0.97, p0.05; LVESD index, OR 0.57, CI 0.40-0.85, p=0.005) were the two independent predictors of post-operative LV functional recovery on multivariate analysis. A cut off value of pre-operative LVESD index=or27.5 mm/m(2) was 85% sensitive and 72% specific in predicting intermediate-term recovery of LV function after AVR (AUC, 0.72, p=0.002).LV functional recovery was evident in majority of aortic stenotic patients with LV dysfunction after aortic valve replacement. A lower prevalence of LV functional recovery in patients with large pre-operative LV end systolic dimension index might signify the loss of contractile reserve and thus predict post-operative functional recovery.