Carmen Ginghină

Morphological and Functional Adaptation of the Maternal Heart during Pregnancy

Background— Pregnancy provides a unique model to study the adaptation of the heart in a physiological situation of transient load changes. The aim of this study was to assess the performance of the left ventricle (LV) in normal, uncomplicated pregnancies while considering the actual LV load and shape. Methods and Results— Serial echocardiographic examinations were performed in 51 women in each pregnancy trimester and 3 to 6 months after delivery. Data from 10 nulliparous, age-matched women were used as the control. Conventional parameters of LV function (ejection fraction) as well as myocardial deformation (strain) were interpreted, taking into consideration maternal hemodynamics and LV shape. Cardiac output increased during pregnancy because of a higher stroke volume in early pregnancy and a late increase in heart rate, whereas total vascular resistance decreased. Progressive development of eccentric hypertrophy was observed, which subsequently recovered postpartum. Sphericity index decreased from the first to the third trimester (1.92±0.17 versus 1.71±0.17) and returned postpartum to values comparable to the control. Although higher LV stroke work was noted toward the third trimester (5.9±1.1 versus 5.3±1.0 Newton meter, P<0.001), ejection fraction showed no significant changes. LV strain decreased significantly in late pregnancy (−19.5±2% to −17.6±1.6%, P<0.001) and returned to baseline values after delivery (−19.5±2%). Conclusions— Pregnancy is a physiological process associated with increased cardiac performance and progressive LV remodeling. These changes are not directly reflected by parameters traditionally considered to describe systolic function, such as ejection fraction and longitudinal deformation. While ejection fraction was insensitive to the functional changes, the transient decrease in longitudinal deformation becomes only plausible when considering the changes in LV geometry.

Stage-related effect of statin treatment on the progression of aortic valve sclerosis and stenosis.

It has been suggested that statins could slow the progression of aortic stenosis (AS), but this hypothesis is still debated and has not been validated in large series of patients by long-term follow-up studies. Moreover, information about the role of statins in patients with different degrees of severity of AS is scarce. From our 1988 to 2007 echocardiographic database, we retrospectively identified all asymptomatic patients with aortic valve sclerosis (abnormal irregular thickening of the aortic valve with a peak aortic velocity [Vmax] > or =1.5 and <2 m/s), mild AS (Vmax > or =2 and <3 m/s), and moderate AS (Vmax > or =3 and <4 m/s), age > or =50 years, and with > or =2 echocardiographic studies > or =2 years apart. Exclusion criteria were moderate/severe aortic regurgitation, bicuspid aortic valve, rheumatic valve disease, and ejection fraction <40%. The final study population consisted of 1,046 patients (mean age 70 +/- 8 years, 587 men); 309 were treated with statins. Mean follow-up duration was 5.6 +/- 3.2 years (range 2 to 19). Progression of AS was slower in patients receiving statins compared with untreated patients in aortic sclerosis (0.04 +/- 0.09 vs 0.07 +/- 0.10 m/s/year, p = 0.01) and mild AS (0.09 +/- 0.15 vs 0.15 +/- 0.15 m/s/year, p = 0.001), but not in moderate AS (0.21 +/- 0.18 vs 0.22 +/- 0.15 m/s/year, p = 0.70). In multivariate analysis only statin therapy, initial Vmax, and dialysis were independently related to progression of aortic valve disease. In conclusion, in a large series of patients with long-term follow-up, statins were effective in slowing the progression of aortic valve disease in aortic sclerosis and mild AS, but not in moderate AS. These results suggest that statin therapy should be taken into consideration in the early stages of this common disease.

Left atrial dysfunction as a correlate of heart failure symptoms in hypertrophic cardiomyopathy.

BACKGROUND Hypertrophic cardiomyopathy (HCM) represents a generalized myopathic process affecting both ventricular and atrial myocardium. We aimed to assess left atrial (LA) function by two-dimensional speckle tracking echocardiography and its relation with left ventricular (LV) function and clinical status in patients with HCM. METHODS We prospectively enrolled 37 consecutive patients with HCM and 37 normal subjects with similar age and gender distribution. Longitudinal LV strain (ε) and LA ε and strain rate (Sr) parameters (systolic, early diastolic, and late diastolic during atrial contraction) were assessed. RESULTS Peak LAε and LA Sr parameters were significantly lower in patients compared with controls (P ≤ .001 for all). In patients, all LA function parameters correlated with LVε (P < .003 for all). Indexed LA volume, LA function parameters, and mitral regurgitation degree were the main correlates of New York Heart Association class; late diastolic strain rate during atrial contraction was the only independent predictor of symptomatic status. CONCLUSION In patients with HCM, LA function is significantly reduced and related to LV dysfunction. Moreover, LA booster pump function emerged as an independent correlate of heart failure symptoms in this setting.

Left ventricular remodelling and torsional dynamics in dilated cardiomyopathy: reversed apical rotation as a marker of disease severity

Decreased left ventricular (LV) rotation and torsion and even reversed systolic apical rotation have been described in patients with dilated cardiomyopathy (DCM). We sought to test in patients with DCM whether reversed apical rotation with loss of LV torsion is related to the extent of LV remodelling and to the severity of LV dysfunction.

Hydroxymethylglutaryl coenzyme-a reductase inhibitors delay the progression of rheumatic aortic valve stenosis a long-term echocardiographic study.

OBJECTIVES This study sought to assess the effect of hydroxymethylglutaryl coenzyme-A reductase inhibitors (statins) on the progression of rheumatic aortic valve stenosis. BACKGROUND The possible role of statins in slowing the progression of degenerative aortic valve stenosis (AS) is still debated. No information about the role of statin treatment in patients with rheumatic AS is available yet. METHODS From our 1988 to 2008 echocardiographic database, we retrospectively identified all patients with rheumatic AS, with a baseline peak aortic velocity >or=1.5 m/s and at least 2 echocardiographic studies >or=2 years apart. Exclusion criteria were: severe aortic regurgitation, bicuspid aortic valve, and left ventricular ejection fraction <40%. RESULTS The study population consisted of 164 patients (30 treated with statins) followed up for 8.5 +/- 4.2 years. Peak aortic velocity at baseline was not different in patients treated with statins versus untreated patients (2.3 +/- 0.8 m/s vs. 2.3 +/- 0.7 m/s, p = 0.84). There were no significant differences in sex, age, or follow-up duration between the 2 groups. Progression of AS severity was slower in patients receiving statins compared with untreated patients (annual change of peak aortic velocity: 0.05 +/- 0.07 m/s/year vs. 0.12 +/- 0.11 m/s/year, p = 0.001). An annual rate of peak velocity progression >or=0.1 m/s was found in 10% of statin-treated patients and in 49% of untreated patients (p < 0.0001). CONCLUSIONS This is the first observation of a positive effect of statin treatment in reducing the progression of rheumatic AS. The underlying mechanisms remain to be clarified.

Echo-Tracking Assessment of Carotid Artery Stiffness in Patients with Aortic Valve Stenosis

Background: There is little information about mechanical properties of large arteries in patients (pts) with aortic stenosis (AS). Methods: Nineteen patients with AS (aortic valve area: 0.88 ± 0.29 cm2) and 24 control subjects without AS but with a similar distribution of risk factors were recruited. β index, pressure‐strain elastic modulus (Ep), arterial compliance (AC), augmentation index (AIx), and local pulse‐wave velocity (PWV) were obtained at the level of right common carotid artery (CCA) by a real time echo‐tracking system. Time to dominant peak of carotid diameter change waveform, corrected for heart rate (tDPc), and maximum rate of rise of carotid diameter (dD/dt) were measured. Systemic arterial compliance (SAC) was also calculated. Parameters of AS severity (mean gradient, valve area, stroke work loss [SWL]) were determined. Results: tDPc was higher in patients with AS than in controls (7.9 ± 0.6 vs. 6.6 ± 0.7, P < 0.0001) while dD/dt was lower (5.3 ± 3.6 mm/s vs. 7.8 ± 2.8 mm/s, P = 0.01). AIx was significantly higher in AS group (32.5 ± 13.6% vs. 20.6 ± 12.2%, P = 0.005) and had a linear correlation both with tDPc (r = 0.63, P < 0.0001) and with dD/dt (r =−0.38, P = 0.01). There was a significant correlation between carotid AC and SAC (r = 0.49, P = 0.03), but only carotid AC was related to SWL (r = 0.51, P = 0.02), while SAC was not (P = 0.26).Conclusions: AIx was the only parameter of arterial rigidity found to be higher in patients with AS than in controls. Carotid AC showed a significant correlation with SAC and it seemed to be more closely related to AS severity than to SAC.

Cardiac structure and function and insulin resistance in morbidly obese patients: does superobesity play an additional role?

Objective: To evaluate the impact of superobesity, defined as body mass index (BMI) ≥50, on cardiac structure and function. Methods: Using echocardiography, we studied 198 asymptomatic patients (mean age 48 ± 13 years, 29.3% were men) with a BMI ≥40. Insulin resistance was measured using the Homeostasis Model Assessment of insulin resistance (HOMA-IR). Patients were divided into 2 groups: morbidly obese (BMI ≥40 and <50; n = 160) and superobese (BMI ≥50; n = 38). Results: There were no significant differences in age, gender, hypertension and diabetes between groups. Superobese patients had higher LV mass (66.0 ± 14.7 vs. 59.9 ± 11.9 g/m2.7, p = 0.007), left ventricular (LV) end-diastolic (33.8 ± 7.7 vs. 31.5 ± 7.1 ml/m2.7, p = 0.041) and end-systolic (12.2 ± 3.6 vs. 10.9 ± 2.8 ml/m2.7, p = 0.016) volumes, left atrial volume (13.8 ± 4.5 vs. 12.2 ± 3.9 ml/m2.7, p = 0.029), peak velocity of transmitral flow in early diastole/early diastolic peak myocardial velocity ratio (9.1 ± 2.6 vs. 8.2 ± 2.2, p = 0.03) and HOMA-IR (9.7 ± 7.3 vs. 7.3 ± 6.5, p = 0.047). LV ejection fraction was similar. Conclusions: Superobesity is associated with insulin resistance and a worse impact on cardiac remodeling and LV diastolic function than morbid obesity. Prospective studies are needed to evaluate whether such further classification of morbid obesity could stratify the cardiovascular risk in these patients more accurately.

Impact of associated significant aortic regurgitation on left ventricular remodeling and hemodynamic impairment in severe aortic valve stenosis.

Objectives: The left ventricular (LV) response to combined pressure and volume overload [aortic stenosis (AS) and aortic regurgitation (AR)] versus pressure overload (isolated AS) has not been systematically studied. We aimed to assess LV remodeling, functional and hemodynamic consequences in patients with mixed aortic valve disease versus patients with isolated AS. Methods: We enrolled 181 patients (67 ± 9 years, 109 men) with severe AS (aortic valve area indexed to body surface area <0.6 cm2/m2) who underwent preoperative cardiac catheterization and a complete echocardiogram. Pulmonary capillary wedge pressure (PCWP), LV end-diastolic pressure (LVEDP) and pulmonary artery pressure (PAP) were measured. Results: One hundred and ten patients (group A) had isolated severe AS (AR 0-1) and 71 patients (group B) had mixed aortic valve disease (severe AS plus AR 2-3). Patients in group B were younger and in a higher New York Heart Association class (p < 0.01). Severity of AS was similar in both groups. Patients in group B had a higher indexed LV mass, a lower LV ejection fraction, and higher PCWP, LVEDP and PAP (all p ≤ 0.01). Conclusions: Patients with severe AS and significant AR are more symptomatic than patients with isolated severe AS. The increased burden due to the combined lesion induces pronounced LV remodeling and more severe hemodynamic consequences.

The left ventricle in aortic stenosis - imaging assessment and clinical implications

Aortic stenosis has an increasing prevalence in the context of aging population. In these patients non-invasive imaging allows not only the grading of valve stenosis severity, but also the assessment of left ventricular function. These two goals play a key role in clinical decision-making. Although left ventricular ejection fraction is currently the only left ventricular function parameter that guides intervention, current imaging techniques are able to detect early changes in LV structure and function even in asymptomatic patients with significant aortic stenosis and preserved ejection fraction. Moreover, new imaging parameters emerged as predictors of disease progression in patients with aortic stenosis. Although proper standardization and confirmatory data from large prospective studies are needed, these novel parameters have the potential of becoming useful tools in guiding intervention in asymptomatic patients with aortic stenosis and stratify risk in symptomatic patients undergoing aortic valve replacement.This review focuses on the mechanisms of transition from compensatory left ventricular hypertrophy to left ventricular dysfunction and heart failure in aortic stenosis and the role of non-invasive imaging assessment of the left ventricular geometry and function in these patients.

Right ventricular remodeling in athletes and in arrhythmogenic cardiomyopathy

Abstract Objective: Changes in right ventricular (RV) structure and function following prolonged endurance training in athletes arise due to its unique anatomy and physiology. Arrhythmogenic cardiomyopathy (AC) should be differentiated from electrical, functional and structural adaptation of the heart in response to repetitive intense physical activity due to the negative contribution of exercise on AC progression and arrhythmic risk. Design: For this review we performed a systematic search of the PubMed database up to October 2017 using terms and keywords pertaining to RV, athlete’s heart (AH), AC, sudden cardiac death. Results: This review summarizes currently available data on the impact of exercise on cardiac structure and function, discusses the debatable hypothesis of exercise-induced RV remodeling, compares the common features and search for distinctive characteristics between AH and AC. Conclusion: Exercise has a more profound impact on the structure and function of the RV than of the left ventricle. Differentiating physiologic RV remodeling following prolonged endurance exercise from subclinical cardiac pathology can be challenging. A multimodality approach is recommended to differentiate between exercise-induced physiological adaptations and cardiomyopathy.