Biomedical subjects

Lorenzo Monserrat

Publications and source records attributed to Lorenzo Monserrat.

23 records · Page 2Linked to original sources

PubMed2002

[Familial dilated cardiomyopathy in patients transplanted for idiopathic dilated cardiomyopathy].

OBJECTIVE: To evaluate the prevalence, clinical features, and pattern of inheritance of familial dilated cardiomyopathy (DCM) in heart transplant patients. PATIENTS AND METHOD: Patients with idiopathic DCM who had undergone heart transplantation were invited to participate. Patients with alcohol abuse were excluded. A clinical evaluation, 12-lead ECG, echocardiogram, blood tests, and DNA extraction were performed in patients and relatives. Familial DCM was defined as the presence of at least one relative with idiopathic DCM. Possible familial DCM was considered when at least one relative had left ventricular enlargement (LVE) (> 112% predicted LVEDD). RESULTS: One hundred and ninety-nine relatives of 43 families were studied. DCM was familial in 11 probands (25.6%) and possibly familial in 11 (25.6%). Fifteen relatives had DCM (7.5%), 26 (13.1%) LVE, and 5 (2.5%) hypertrophic cardiomyopathy. The pattern of inheritance was autosomal dominant in most families. Five probands (3 with familial DCM) had antecedents of consanguinity and possible recessive inheritance. Six probands (14%, 1 with familial DCM) had relatives with conduction system defects. Creatine kinase was moderately increased in 9 relatives (4.5%), 3 of them with LVE. Fifteen patients had at least moderate alcohol intake. Three of them had familial DCM (relatives without alcohol abuse) and 6 had possible familial DCM. CONCLUSIONS: The prevalence of familial DCM is high in patients who undergo heart transplant. Left ventricular enlargement, conduction system abnormalities, and elevated creatine kinase may be early markers of familial disease. Hypertrophic cardiomyopathy is present in some relatives of patients with idiopathic DCM. Familial DCM is present in patients with a previous diagnosis of alcoholic DCM.

Biomarkers↗

PubMed2002

Effect of left ventricular global systolic function, mitral regurgitation, and left ventricular inflow pattern on exercise echocardiography results.

Diagnosis of coronary artery disease (CAD) by exercise echocardiography is usually based on rest or exercise-induced regional wall-motion abnormalities. Mitral regurgitation (MR), left ventricular (LV) global systolic function, and LV inflow measurements can be assessed during exercise echocardiography; however, their diagnostic value has not been analyzed consistently. Treadmill exercise echocardiography and coronary angiography were performed in 120 patients (94 male, 26 female; mean age 61 +/- 10 years [+/- 1 SD]) to evaluate known or suspected CAD. Positive exercise echocardiography was defined either as a rest- or exercise-induced regional wall-motion abnormalities. An abnormal response of LV ejection fraction (EF), LV volumes, MR (as assessed by color Doppler), and LV inflow pattern was defined as a fall in LVEF, a LV end-diastolic volume increase, a LV end-systolic volume increase, a new or increased MR, or a change from an impaired relaxation pattern (E < A) to a "pseudonormalized" pattern (E > A) from rest to exercise, respectively. CAD (> or = 50% luminal narrowing in at least one vessel) was found in 89 (74%) patients. EE-based regional wall-motion abnormality analysis was positive in 95 (79%) patients and negative in 25 (21%) patients. Feasible images for regional wall-motion abnormalities, LVEF and volumes, LV inflow, and MR measurements were acquired in 90% of patients. Regional wall-motion abnormality analysis and LVEF decrease provided the greatest sensitivities for CAD (94% and 75%, respectively), while the highest specificity was given by a new or increased MR (90%), the development of a pseudonormalized pattern (88%), and the appearance of angina (87%). A positive electrocardiogram (ECG) finding in patients with interpretable ECGs provided good sensitivity and specificity (67% and 85%, respectively). In conclusion, a complete rest and exercise Doppler echocardiography approach is feasible in most patients. Regional wall-motion abnormalities are the most accurate exercise echocardiography variable for diagnosing CAD, whereas exercise ECG remains a good test in patients with interpretable ECGs. Exercise echocardiography, exercise ECG, newly developed or increased MR, and change to a pseudonormalized LV inflow pattern are highly specific.

Aged↗

PubMed2002

Feasibility of pulsed-Doppler tissue imaging of the interventricular septum during exercise echocardiography.

BACKGROUND: A limitation of exercise echocardiography (EE) is its semiquantitative approach in analyzing wall-motion abnormalities. However, pulsed-Doppler tissue imaging is capable of a systolic and diastolic regional quantitative assessment. METHODS: To investigate the feasibility of performing pulsed-Doppler tissue imaging sampling of the basal left ventricular (LV) septum during EE, we studied 105 consecutive patients (71 men, 34 women, aged 61 +/- 11 years). Harmonic two-dimensional (2-D) echocardiography was performed at rest and peak EE, whereas pulsed-Doppler tissue imaging was performed at rest and immediately after EE. Adequate recordings for peak systolic velocity (Vs) were possible in all patients, but peak early diastolic (Ve) and peak late diastolic (Va) velocities were possible in 78 (74%) patients. Positive 2-D echocardiography was considered as infarction or an ischemic response. RESULTS: Forty-five (43%) patients (Group 1) had wall-motion abnormalities involving the left anterior descending artery (LAD) territory (29 with ischemia, 11 with ischemia and necrosis, and 5 with necrosis), 21 (20%) (Group 2a) had wall-motion abnormalities involving the left circumflex (LCX) and/or the right coronary artery (RCA) territories, and 39 (37%) (Group 2b) had normal EE. Heart rate increased from 72 +/- 17 beats/min to 143 +/- 18 beats/min (P < 0.0001) and systolic blood pressure from 129 +/- 19 mmHg to 174 +/- 26 mmHg (P < 0.001). Coronary angiography was performed in 30 (29%) patients, 29 of whom had positive findings on EE. LAD or diagonal branch coronary artery disease (CAD) (> or = 50% luminal narrowing) was present in 22 patients, 10 of whom had proximal severe stenosis (> or = 70% luminal narrowing). Vs increase was significatively lower in Group 1 (40 +/- 35%, from 6.0 +/- 1.5 cm/sec to 8.1 +/- 2.2 cm/sec) than Group 2a (75 +/- 35%, from 6.3 +/- 1.4 cm/sec to 10.8 +/- 2.1 cm/sec, P < 0.0001) and Group 2b (64 +/- 27%, from 6.7 +/- 1.3 cm/sec to 10.9 +/- 2.0 cm/sec, P < 0.001). Ve was not different at rest and at postexercise between groups. Va was similar at rest but higher at postexercise in Group 2b than Group 1 (11.8 +/- 2.3 cm/sec vs 10.3 +/- 3.0 cm/sec, P < 0.05). Failure to achieve Vs > or = 9.5 cm/sec after exercise was found to be the more accurate limit to detect necrosis or ischemia in the LAD territory according to EE criteria (sensitivity 76%, specificity 78%). When analysis was limited to the 30 patients who underwent angiography, we found that the 10 patients with proximal severe LAD or diagonal branch stenosis showed blunted increases in Vs (increase 9.4 +/- 19%, from 6.5 +/- 1.2 cm/sec at rest to 7.4 +/- 1.7 cm/sec at post-EE; P = 0.17) in contrast to the 20 patients having moderate or nonsignificant stenosis (increase 31 +/- 20%, from 6.2 +/- 1.5 cm/sec at rest to 9.3 +/- 1.8 cm/sec at post-EE, P < 0.0001). A failure to increase Vs > or = 30% had a sensitivity of 90% and a specificity of 80% in detecting proximal severe stenosis. CONCLUSION: Pulsed-Doppler tissue imaging sampling of the LV septum is feasible technically during EE and allows quantification of the regional response. This method may be accurate for detecting proximal severe stenosis in vessels supplying the LAD territory.

Adult↗

PubMedDate not supplied

MRI of subendocardial perfusion deficits in isolated left ventricular noncompaction.

Ventricular noncompaction is a rare unclassified cardiomyopathy due to intrauterine arrest of compaction of the loose interwoven meshwork. It is characterized by markedly irregular endocardial surfaces with prominent trabeculations and intertrabecular recesses. Patients are asymptomatic or present with depressed ventricular function, ventricular arrhythmia, and systemic embolism. Areas of restricted myocardial perfusion have been previously documented by scintigraphy and positron emission tomography. This report documents a case of isolated left ventricular noncompaction with subendocardial perfusion deficits on MRI.

Adult↗

PubMedDate not supplied

Magnetic resonance imaging of delayed enhancement in hypertrophic cardiomyopathy: relationship with left ventricular perfusion and contractile function.

PURPOSE: The aim of the study was to analyze the relationship between myocardial delayed enhancement, first-pass perfusion, and contractile function in hypertrophic cardiomyopathy (HCM) patients, using MR. METHODS: Fifty-three patients diagnosed with HCM were prospectively examined using a 1.5-T MR unit. Multiphase gradient-echo sequences were performed to study global left ventricular function, wall thickness, and left ventricular mass. Myocardial tissue tagging was conducted to evaluate contractile function. T1-weighted inversion-recovery sequences were obtained at rest to study myocardial contrast enhancement at first pass and delayed enhancement 10 minutes later. RESULTS: Delayed enhancement found in 30 patients (56.6%) was most commonly seen in hypertrophic segments. Nine patients exhibited delayed enhancement in segments with normal wall thickness (<15 mm). Sixteen patients (30.1%) showed first-pass perfusion defects at rest, which were associated with significantly lower stroke volume (P<0.05) and lower cardiac output (P<0.01). The hypokinetic segments found in 16 patients (30.1%) were significantly thicker at end diastole (P<0.01). Delayed enhancement correlated positively with perfusion defects (r=0.5, P<0.01) and hypokinetic segments (r=0.3, P<0.05). CONCLUSION: Delayed myocardial enhancement is most commonly found in hypertrophic segments but also can be seen in segments with normal wall thickness. Perfusion defects at rest and impaired contractile function are related abnormalities with delayed myocardial enhancement. Further studies are necessary to assess the role of myocardial tagging, first-pass perfusion, and delayed enhancement in risk stratification for patients with HCM.

Adolescent↗