Persisting effect of Ca(2+)-channel blockers on left ventricular function in hypertrophic cardiomyopathy after 14 years' treatment

Ca(2+)-channel blockers of the verapamil type have been reported to exert a beneficial effect on clinical symptoms and survival rates in hypertrophic cardiomyopathy. The effects of verapamil have been attributed predominantly to an improved diastolic filling. It is unknown whether an effect on diastolic filling persists in these patients after long-term treatment. Fourteen patients (12 men, 2 women, median age fifty-one [thirty-two to fifty-five] years) with hypertrophic cardiomyopathy were included in the study. Patients had been treated with verapamil 240-480 mg/d or gallopamil 150-200 mg/d for fourteen (seven to seventeen) years. The effect of a withdrawal of Ca(2+)-channel blockers on parameters of left ventricular diastolic function was evaluated at rest and during exercise in patients with hypertrophic cardiomyopathy after long-term therapy. Investigations were performed at rest and during supine ergometric exercise during ongoing Ca(2+)-channel blocking therapy and after five (four to nine) days' withdrawal (control). Pulsed Doppler echocardiography was used to record diastolic mitral flow profiles from an apical four-chamber view. Withdrawal of Ca(2+)-channel blockers of the phenylalkylamine type after long-term treatment of hypertrophic cardiomyopathy resulted in a significant reduction of early diastolic inflow velocity at rest and during exercise. In conclusion, these results indicate a persistent improvement of early diastolic filling by Ca(2+)-channel blockers even after long-term treatment.     

Prognostic importance of left ventricular diastolic filling velocity profiles in dilated cardiomyopathy

To determine the prognostic importance of pulsed Doppler-derived left ventricular diastolic filling velocity profiles and the relationship between Doppler variables and clinical functional status, the follow-up outcome of 58 patients with dilated cardiomyopathy and symptoms of left ventricular dysfunction was analysed. During a mean follow-up period of 31.2 +/- 12.8 months, 23 died of either progressive pump failure or sudden death. Peak early filling velocity (E) was higher and late atrial filling velocity (A) lower in nonsurvivors than in survivors. The E/A ratio was higher and the deceleration time (DT) of early diastole shorter in nonsurvivors. The mortality was significantly higher in patients with an E/A ratio > 2 or a DT < 150 ms than in those without. Repeated Doppler echocardiographic examinations in 31 of 35 survivors after intense treatment showed decreased E, increased A, reduced E/A ratio and prolonged DT in 18 patients with clinical functional improvement, whereas these measurements were unaltered in the remaining 13 patients whose functional status was unchanged or deteriorated. This study suggests that pulsed Doppler-derived left ventricular diastolic filling variables may be important predictors of outcome in dilated cardiomyopathy and provide useful measures in observing the effects of therapy during long-term follow-up of the patients.     

Value of radionuclide ventriculography and magnetic resonance imaging in the diagnosis of constrictive pericarditis

In suggestive clinical presentations, the diagnosis of constrictive pericarditis is confirmed by the haemodynamic findings of impaired ventricular filling (diastole). In this study of 15 patients with pure constrictive pericarditis, the diagnosis value of two non-invasive techniques little used in this indication until now was examined: radionuclide ventriculography (RV) and magnetic resonance imaging (MRI). The RV provides a "functional" diagnosis through the analysis of global and segmental left ventricular filling whilst MRI provides anatomical details of the pericardial thickening. Diastolic dysfunction on RV presented as an increased early diastolic filling time as shown by a shortening of the interval to third filling T1/3R (p < 0.0001), an increased peak diastolic E wave velocity (p < 0.01) and early onset (p < 0.001), increased one third (FR 1/3) and mid (FR 1/2) diastolic filling fractions (p < 0.01) and of the E wave velocity to maximal systolic ejection velocity (S) ration (p < 0.01). The atrial contribution to filling in end diastole decreased (NS). Asynchronous filling, shown by dispersion of the times of onset of segmental early diastolic E peak velocities (delta tE) or of one third diastolic filling delta T1/3R, decreased. Seven patients underwent MRI. Pericardial thickening was present in all patients. The pericardium varied from 6 to 14 mm thick (normal 2.5 +/- 0.7 mm), without any systolo-diastolic variation. The thickening was seen as a dark low intensity signal, indicating the fibro-calcific character of the tissues. Sagittal and coronal views clearly demonstrated the non-uniformity of pericardial thickening.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transient hypertrophic subaortic stenosis in infants of diabetic mothers

Three newborn infants with congestive heart failure had hemodynamic, angiographic, and echocardiographic features of hypertrophic subaortic stenosis (hypertrophic obstructive cardiomyopathy). Treatment with digitalis and diuretic drugs was ineffective, but improvement occurred when these agents were withheld in one patient, and when treatment with propranolol was begun in two patients. Echocardiography was helpful in establishing the diagnosis in two patients and showed resolution of the condition during the first six months of life. Serial cardiac catheterizations confirmed resolution of the outflow obstruction in the third patient. Family studies revealed no evidence of familial cardiomyopathy, but the mothers of two infants had insulin-dependent diabetes mellitus and the mother of the third was presumed to be prediabetic.     

Hypothesis of the compression of morbidity: an example of theoretical development in epidemiology]

To assess the usefulness of the tissue Doppler imaging variables for the evaluation of left ventricular (LV) systolic function, we compared variables obtained by the pulsed Doppler method with the LV ejection fraction (%EF) and the maximum value for the first derivative of LV pressure (peak dP/dt). We examined 65 patients, including 15 patients with noncardiac chest pain, 15 with ischemic heart disease, 15 with dilated cardiomyopathy, 10 with hypertensive heart disease, and 10 with asymmetric septal hypertrophic cardiomyopathy. The subendocardial systolic wall motion velocity patterns were recorded for LV posterior wall and ventricular septum in the parasternal LV long-axis view. The peak dP/dt was significantly lower in the hypertensive heart disease, hypertrophic cardiomyopathy, and dilated cardiomyopathy groups. The peak systolic velocity was lower and the time from the electrocardiographic Q wave to the peak of the systolic wave for the posterior wall was longer in the hypertensive heart disease (5.9 +/- 0.5 cm/sec and 215 +/- 21 msec, respectively), hypertrophic cardiomyopathy (6.2 +/- 0.9 cm/sec and 217 +/- 17 msec, respectively), and dilated cardiomyopathy (5.2 +/- 0.8 cm/sec and 235 +/- 26 msec, respectively) groups than in the noncardiac chest pain (7.7 +/- 0.9 cm/sec and 187 +/- 24 msec, respectively) and the ischemic heart disease (7.6 +/- 0.8 cm/sec and 184 +/- 22 msec, respectively) groups. In all groups, the peak systolic velocity and the time from the electrocardiographic Q wave to the peak of the systolic wave for the posterior wall correlated directly and inversely, respectively, with the %EF (r = 0.59, p < 0.0001; r = -0.59, p < 0.0001) and the peak dP/dt (r = 0.75, p < 0.0001; r = -0.68, p < 0.0001). Both tissue Doppler variables for the ventricular septum did not correlate with the %EF but roughly correlated with peak dP/dt. We conclude that the systolic LV wall motion velocity parameters obtained by pulsed tissue Doppler imaging may be useful for noninvasive evaluation of global LV systolic function in patients with no regional asynergy.     

Imaging strategies for brain tumours

Growth factors have been shown to be associated with primary hypertrophic cardiomyopathy. Octreotide, a long acting somatostatin analogue, can prevent the stimulating effect of growth factors and decrease the left ventricular mass in patients with acromegaly. In the light of these results, three patients with primary hypertrophic cardiomyopathy were treated with subcutaneous octreotide (50 micrograms three times a day during the first week and 100 micrograms twice a day for the following three weeks). Initially, two patients were in New York Heart Association class II in and one was in class III. At the end of a four week treatment session all were in class I. There were significant decreases in left ventricular posterior wall thickness, interventricular septum thickness, and left ventricular mass in all three patients. Both left ventricular end diastolic and end systolic diameters had increased in all of the patients at the end of the fourth week. Two of three patients showed improved diastolic filling: their hyperdynamic systolic performance returned to normal. No side effects were observed during octreotide treatment. The considerable improvement obtained with the short term octreotide treatment in patients with primary hypertrophic cardiomyopathy seems promising.     

Evaluation of left ventricular early diastolic performance by color tissue Doppler imaging of the mitral annulus

A noninvasive assessment of left ventricular (LV) diastolic performance by tissue Doppler imaging was performed in 56 patients (8 patients with atypical chest pain, 42 with coronary artery disease with a previous myocardial infarction, and 6 without a previous myocardial infarction) who underwent cardiac catheterization. Mitral annular velocity (MAV) during early ventricular diastole was obtained by M-mode color tissue Doppler imaging at the posterior corner of the mitral annulus. In each patient, the negative peak of the first derivative of LV pressure decay (peak -dP/dt) and a time constant of LV relaxation (tau) were calculated from the LV pressure waves obtained by a catheter-tip micromanometer. LV end-systolic volume index was measured from contrast left ventriculography. MAV during early diastole was significantly correlated with tau (r = -0.73, p <0.001), peak -dP/dt (r = 0.58, p <0.001), and LV end-systolic volume index (r = -0.63, p <0.001). On multivariate regression analysis with MAV during early diastole, tau and LV end-systolic volume index were selected as prime determinants (r = 0.80, p <0.001). These findings suggest that MAV during early diastole has a direct relation to LV elastic recoil as well as to LV relaxation. MAV during early diastole gives important information regarding LV behavior in late systole to early diastole where LV early diastolic performance is determined.     

Is there increased sympathetic activity in patients with hypertrophic cardiomyopathy?

OBJECTIVES: This study aimed to assess autonomic nervous system activity in patients with hypertrophic cardiomyopathy. BACKGROUND: Patients with hypertrophic cardiomyopathy are traditionally thought to have increased sympathetic activity. However, convincing evidence is lacking. METHODS: Heart rate variability was assessed from 24-h ambulatory electrocardiographic (Holter) recordings in 31 patients with hypertrophic cardiomyopathy and 31 age- and gender-matched normal control subjects in a drug-free state. Spectral heart rate variability was calculated as total (0.01 to 1.00 Hz), low (0.04 to 0.15 Hz) and high (0.15 to 0.40 Hz) frequency components using fast Fourier transformation analysis. RESULTS: There was a nonsignificant decrease in the total frequency component of heart rate variability in patients with hypertrophic cardiomyopathy compared with that of normal subjects (mean +/- SD 7.24 +/- 0.88 versus 7.59 +/- 0.57 ln[ms2], p = 0.072). Although there was no significant difference in the high frequency component (5.31 +/- 1.14 versus 5.40 +/- 0.91 ln[ms2], p = 0.730), the low frequency component was significantly lower in patients than in normal subjects (6.25 +/- 1.00 versus 6.72 +/- 0.61 ln[ms2], p = 0.026). After normalization (i.e., division by the total frequency component values), the low frequency component was significantly decreased (38 +/- 8% versus 43 +/- 8%, p = 0.018) and the high frequency component significantly increased (16 +/- 6% versus 12 +/- 6%, p = 0.030) in patients with hypertrophic cardiomyopathy. The low/high frequency component ratio was significantly lower in these patients (0.94 +/- 0.64 versus 1.33 +/- 0.55, p = 0.013). In patients with hypertrophic cardiomyopathy, heart rate variability was significantly related to left ventricular end-systolic dimension and left atrial dimension but not to maximal left ventricular wall thickness. No significant difference in heart rate variability was found between 14 victims of sudden cardiac death and 10 age- and gender-matched low risk patients. CONCLUSIONS: Our observations suggest that during normal daily activities, patients with hypertrophic cardiomyopathy experience a significant autonomic alteration with decreased sympathetic tone.     

Left ventricular diastolic stiffness in dogs with congestive cardiomyopathy and volume overload

Mean functional diastolic stiffness, an estimate of the left ventricular resistance to filling during diastole, was measured in 10 normal dogs, 7 dogs with diseases causing volume overload (patent ductus arteriosus and primary mitral valve insufficiency), and 4 dogs with idiopathic congestive cardiomyopathy. It was measured as the increase in pressure during diastole (deltaP), divided by the corresponding increase in volume (deltaV). The pressure was measured at cardiac catheterization, and the volume was derived by a cineangiocardiographic method. There was no increase in diastolic stiffness of the hearts with volume overload compared with the normal hearts, but those with cardiomyopathy had a large increase, although the end-diastolic volumes in cardiomyopathy were generally less than in volume overload.     

Effects of postural changes on left atrial function in patients with hypertrophic cardiomyopathy

BACKGROUND: We assessed left atrial function in normal subjects and in patients with hypertrophic cardiomyopathy (HCM) by using Doppler echocardiography at the supine position and after sudden standing. METHODS AND RESULTS: Twenty-seven patients with hypertrophic obstructive cardiomyopathy (HOCM), 17 patients with HCM, and 35 normal subjects were studied. From the transmitral Doppler flow velocities, peak early and late (E and A) waves, E/A ratio, and time velocity integrals (Ei and Ai) were calculated. Left atrial active contribution (LAAC) was assessed as the ratio Ei/(Ei + Ai). Furthermore, isovolumetric relaxation time (IVRT) was estimated by means of Doppler echocardiography. In the supine position, the E/A ratio was similar in the 3 groups. Conversely, LAAC was significantly higher in patients with HOCM (24.4 +/- 2.0) and in patients with HCM (23.3 +/- 3.3) compared with normal subjects (20.3 +/- 2.3, P <.001 and P <.05, respectively). After sudden standing, LAAC increased significantly in normal subjects by 11%, in patients with HOCM by 24%, and in patients with HCM by 13% (P <.001). Similarly, IVRT increased significantly in all study groups (P <. 001). By using stepwise forward multiple linear regression analysis, we found that LAAC was associated with age, IVRT, and body mass index in the supine position and with diastolic blood pressure and IVRT in the standing position. CONCLUSIONS: Left atrial contribution to left ventricular filling was increased after sudden changes of posture in normal subjects and in patients with HOCM or HCM.     

Left ventricular diastolic function in patients with type-I diabetes mellitus (based on pulsed Doppler echocardiographic data)

Diastolic function was studied of left ventricle by pulse Doppler echocardiography in 42 patients with type I diabetes mellitus (DM) and 46 essentially healthy individuals. In DM patients diastolic function was manifested by rise in peak velocity of atrial filling, decrease in ratio of peak velocity of early filling to that of late one, increase in left ventricular end-diastolic pressure. The findings available suggest the atrial phase has an important part in the structure of diastole in DM patients because of a combined influence of tachycardia and increased rigidity of left ventricular myocardium. Values for early filling in the patients did not differ from those in controls. A conclusion is drawn to the effect that in DM patients tachycardia and hypercatecholaminemia may partly mask disturbances in relaxation.     

Left ventricular diastolic pressure-volume relations in man

Diastolic function of the left ventricle was analysed in patients with different cardiac diseases: acute and chronic volume overload (in aortic and mitral incompetence), pressure overload and inappropriate ventricular hypertrophy (aortic stenosis and hypertrophic cardiomyopathy), congestive cardiomyopathy, and constrictive pericarditis. Most patients were receiving digitalis therapy at the time of study. A constant exponential relation between pressure and volume was assumed, and pressure-volume curves were constructed from two points: the instantaneous pressure-volume relation at beginning-diastole and at end-diastole. The determinants of left ventricular end-diastolic pressure were studied. Left ventricular end-diastolic pressure depended on the beginning-diastolic pressure and volume (O point), the slope of the pressure-volume curve (m), and the volume which distended the ventricle in diastole. In chronic volume loading and in congestive cardiomyopathy the curves were flatter than normal, so that left ventricular end-diastolic pressure was only slightly increased despite the large volume filling the ventricle. In pressure overload and in constrictive pericarditis the curves were steeper than normal. Acute changes in volume were accomplished by a shift up or down the pressure-volume curve but in these patients the slope was not altered: the ventricle had not had time to adapt and end-diastolic pressure was greatly increased.     

Abnormal coronary flow dynamics at rest and during tachycardia associated with impaired left ventricular relaxation in humans: implication for tachycardia-induced myocardial ischemia

OBJECTIVES: This study attempted to clarify the effect of ventricular relaxation abnormalities on coronary flow dynamics at rest and during tachycardia in humans. BACKGROUND: Ventricular relaxation abnormality has been demonstrated in animals to have an adverse impact on early diastolic coronary flow dynamics. However, this relation has not been established in humans. Even if the adverse effect were latent at rest, it might become evident during tachycardia because tachycardia reduces coronary flow reserve and facilitates the production of myocardial ischemia. METHODS: Doppler phasic left coronary flow velocity pattern was obtained at rest and during tachycardia in 23 patients without coronary stenosis. The time constant of left ventricular isovolumic pressure (tau) was used to assess ventricular relaxation. RESULTS: The time to peak flow velocity of the diastolic coronary flow wave was longer, and the fraction of the first third of diastolic coronary flow was smaller, in patients with a longer tau (r = 0.58, p < 0.01; r = -0.44, p < 0.05), indicating a close relation between early diastolic coronary flow dynamics and ventricular relaxation. Although rapid atrial pacing yielded an increase in the coronary flow velocity integral per minute in all patients, diastolic coronary flow velocity integral per minute increased in 9 patients with a normal (< or = 40 ms) tau at rest but decreased in 14 patients with a longer (> 40 ms) tau at rest. CONCLUSIONS: Impaired left ventricular relaxation was associated with decreased coronary flow in early diastole at rest and decreased coronary flow throughout diastole during tachycardia in patients without coronary stenosis. These findings may provide more insight into the mechanism of tachycardia-induced subendocardial ischemia in patients with impaired ventricular relaxation but without concomitant coronary stenosis.     

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease

OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.     

A primary intervention program (pilot study) for Mexican American children at risk for type 2 diabetes

Diastolic dysfunction is common in hypertrophic cardiomyopathy (HC). Previous studies suggest that Doppler transmitral flow velocity profiles, and the left atrial (LA) M-mode echogram can be used noninvasively to evaluate left ventricular (LV) diastolic function. However, this has not been proved in HC. In this study we determined the relation of Doppler transmitral flow velocity profiles and the LA M-mode echograms to invasive indexes of LV diastolic function in patients with HC. We studied 25 patients with HC, while off drugs, and calculated LA global and active fractional shortening and the slope of both early and late displacement of the posterior aortic wall during LA emptying by M-mode echocardiography. We calculated peak velocity of early (E) and atrial (A) filling, E to A ratio, and E-wave deceleration time by pulsed Doppler echocardiography, and simultaneous radionuclide angiography, LV pressures, time constant of isovolumic relaxation tau, and the constant of chamber stiffness k by cardiac catheterization. The time constant of isovolumic relaxation tau correlated with the slope of early posterior aortic wall displacement (r = 0.59; p <0.01). LV end-diastolic pressure correlated with global LA fractional shortening (r = -0.75; p <0.001); the constant of chamber stiffness k correlated with active LA fractional shortening (r = -0.53; p <0.02). In a subset of 13 patients, in whom echocardiography and cardiac catheterization were performed simultaneously, similar results were found. LA M-mode recordings provide a more reliable noninvasive assessment of diastolic function in HC than mitral Doppler indexes.     

The study of the third heart sound in relation to the left ventricular filling and wall movement by echocardiography

The left ventricular filling and wall movement were investigated in subjects with a third heart sound or ventricular gallop by echocardiography. Nine patients with ventricular gallop, who had left ventricular volume overload disease, and 6 normal subjects with a third heart sound had higher normalized peak rate of increase of the left ventricular dimension (peak dD/dT/D) than 10 normal subjects without a third heart sound (p less than 0.01). The normalized lengthening rate in the rapid filling phase was also higher in patients with ventricular gallop than in normal subjects without a third heart sound (p less than 0.05). The time from the second heart sound to peak dD/dT/D and rapid filling time did not show statistically significant values between subjects with ventricular gallop or a third heart sound and those without a third heart sound. These results suggest that higher peak filling, larger filling volume in the rapid filling phase and more abrupt cessation of the outward movement of the left ventricular wall may be a cause of the production of ventricular gallop in patients with left ventricular volume overload and of the physiological third heart sound.     

Impaired heart rate variability in patients with symptomatic NYHA class II-III hypertrophic cardiomyopathy

Power spectral analysis of heart rate variability was performed to assess cardiac autonomic function using Holter monitoring in 19 hospitalized patients with symptomatic NYHA class II-III hypertrophic cardiomyopathy (sHCM), 20 ambulatory patients with asymptomatic NYHA class I hypertrophic cardiomyopathy (asHCM) and 20 normal control subjects. Power spectral analysis decomposed the heart rate variability into high-frequency power (HF: 0.15-0.40 Hz) and low-frequency power (LF: 0.04-0.15 Hz). HF was corrected by mean RR intervals (CCVHF). CCVHF values and LF/HF ratios were used as indices of vagal and sympathetic modulations, respectively. The sHCM group demonstrated no significant elevation in CCVHF during the nighttime as compared to the daytime, while asHCM and control groups showed significant CCVHF elevation during the nighttime (p < 0.05-0.01). The nighttime CCVHF, therefore, was significantly lower in the sHCM group than in the control or asHCM group (sHCM, 1.08 +/- 0.36%; control, 1.60 +/- 0.57%; asHCM 1.82 +/- 0.77%; sHCM vs. control or sHCM vs. asHCM, p < 0.01). All of these three groups showed significant reduction in LF/HF ratio during the nighttime as compared to the daytime (p < 0.01). However, the reduction in the sHCM group was not as great as that in the control group and there was a significant difference between the sHCM and control group (2.01 +/- 1.58 vs. 1.08 +/- 0.65, p < 0.05). Two patients in the sHCM group, who later died suddenly, demonstrated very low CCVHF throughout a 24-hour period (0.2-0.8%). Both vagal and sympathetic impairment with a predominance of vagal abnormalities is suggested in patients with symptomatic NYHA class II or III hypertrophic cardiomyopathy.     

Detection of hepatitis C virus RNA from the heart of patients with hypertrophic cardiomyopathy

We investigated hepatitis C virus (HCV) infection in 35 patients with hypertrophic cardiomyopathy and 40 patients with ischemic heart disease who were consecutively admitted to our hospital. Frequency of positive anti-HCV antibody was significantly higher in patients with hypertrophic cardiomyopathy (6 of 35 patients, 17.1%) than that in patients with ischemic heart disease (1 of 40 patients, 2.5%, p = 0.036). In three of these six patients with hypertrophic cardiomyopathy, HCV RNA was detected in myocardial tissue. In two of these three patients, HCV RNA was detected from biopsy and autopsy specimens of the ventricles, but not in the serum, suggesting that HCV may replicate in myocardial tissue and may be relevant to ventricular hypertrophy. Thus, HCV infection may play a role in the development of hypertrophic cardiomyopathy.     

Differences in myocardial velocity gradient measured throughout the cardiac cycle in patients with hypertrophic cardiomyopathy, athletes and patients with left ventricular hypertrophy due to hypertension

OBJECTIVES: We sought to compare the myocardial velocity gradient (MVG) measured across the left ventricular (LV) posterior wall during the cardiac cycle between patients with hypertrophic cardiomyopathy (HCM), athletes and patients with LV hypertrophy due to systemic hypertension and to determine whether it might be used to discriminate these groups. BACKGROUND: The MVG is a new ultrasound variable, based on the color Doppler technique, that quantifies the spatial distribution of transmyocardial velocities. METHODS: A cohort of 158 subjects was subdivided by age into two groups: Group I (mean [+/-SD] 30 +/- 7 years) and Group II (58 +/- 8 years). Within each group there were three categories of subjects: Group Ia consisted of patients with HCM (n = 25), Group Ib consisted of athletes (n = 21), and Group Ic consisted of normal subjects; Group IIa consisted of patients with HCM (n = 19), Group IIb consisted of hypertensive patients (n = 27), and Group IIc consisted of normal subjects (n = 33). RESULTS: The MVG (mean [+/-SD] s-1) measured in systole was lower (p < 0.01) in patients with HCM (Group Ia 3.2 +/- 1.1; Group IIa 2.9 +/- 1.2) compared with athletes (Group Ib 4.6 +/- 1.1), hypertensive patients (Group IIb 4.2 +/- 1.8) and normal subjects (Group Ic 4.4 +/- 0.8; Group IIc 4.8 +/- 0.8). In early diastole, the MVG was lower (p < 0.05) in patients with HCM (Group Ia 3.7 +/- 1.5; Group IIa 2.6 +/- 0.9) than in athletes (Group Ib 9.9 +/- 1.9) and normal subjects (Group Ic 9.2 +/- 2.0; Group IIc 3.6 +/- 1.5), but not hypertensive patients (Group IIb 3.3 +/- 1.3). In late diastole, the MVG in patients with HCM (Group Ia 1.3 +/- 0.8; Group IIa 1.4 +/- 0.8) was lower (p < 0.01) than that in hypertensive patients (Group IIb 4.3 +/- 1.7) and normal subjects (Group IIc 3.8 +/- 0.9). An MVG < or = 7 s-1, as a single diagnostic approach, differentiated accurately (0.96 positive and 0.94 negative predictive value) between patients with HCM and athletes when the measurements were taken during early diastole. CONCLUSIONS: In both age groups, the MVG was lower in both systole and diastole in patients with HCM than in athletes, hypertensive patients or normal subjects. The MVG measured in early diastole in a group of subjects 18 to 45 years old would appear to be an accurate variable used to discriminate between HCM and hypertrophy in athletes.     

Left ventricular diastolic function in infants, children, and adolescents. Reference values and analysis of morphologic and physiologic determinants of echocardiographic Doppler flow signals during growth and maturation

OBJECTIVES: The aim of this study was to set up reference values for Doppler flow-derived left ventricular filling parameters and to evaluate physiologic determinants of changes in signal expression related to maturation. BACKGROUND: In left ventricular diastolic function studies, age-related modulations in signal expression are observed. Assuming degenerative myocardial changes to be absent during childhood and adolescence, the determinants of these modulations must be different from those suspected in adults. METHODS: Pulsed wave Doppler signals from the mitral valve tip region were recorded in 329 healthy subjects aged 2 months to 39 years. Multiple linear regression was used to evaluate statistical relations between Doppler flow signals and stroke volume in the mitral valve area. RESULTS: Increasing early filling time velocity integral throughout maturation caused a decrease in atrial filling fraction from 0.34+/-0.06 to 0.24+/-0.04 (p < 0.005). Peak flow velocities during atrial systole decreased from infancy to adolescence (66+/-15 to 41+/-10 cm/s). Main effects on signal modulation were caused by heart rate, stroke volume and mitral ring area with a linear model fit (R2) of 0.79 for early filling phase (E)-time velocity integral, 0.6 for atrial filling phase peak velocity 0.84 for total E duration and 0.73 for E deceleration time. Atrial filling phase-time velocity integral, albeit significantly dependent on heart rate, was stable throughout growth. CONCLUSIONS: During infancy and childhood, the stroke volume crossing the mitral valve is a main modulator for early filling phase (E)-time velocity integral and diastolic time intervals during early filling, whereas atrial filling phase parameters are mainly dependent on heart rate. This results in a more pronounced atrial filling during infancy and childhood.