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PubMed1993

Differentiation of constrictive pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow.

OBJECTIVES: The purpose of this study was to test the utility of measuring respiratory variation in pulmonary venous flow by transesophageal echocardiography. BACKGROUND: Respiratory variation of atrioventricular and central venous flow velocities by Doppler echocardiography has been used to differentiate constrictive pericarditis from restrictive cardiomyopathy. METHODS: We performed pulsed wave Doppler transesophageal echocardiography of the left or right pulmonary veins in 31 patients with diastolic dysfunction. Fourteen patients had constrictive pericarditis, and 17 had restrictive cardiomyopathy. We measured the pulmonary venous peak systolic and diastolic flow velocities and the systolic/diastolic flow ratio with transesophageal echocardiography during expiration and inspiration. The percent change in Doppler flow velocity from expiration to inspiration (%E) was calculated. RESULTS: Pulmonary venous peak systolic flow in both inspiration and expiration was greater in constrictive pericarditis than in restrictive cardiomyopathy. The %E for peak systolic flow tended to be higher in constrictive pericarditis (19% vs. 10%, p = 0.09). In contrast, pulmonary venous peak diastolic flow during inspiration was lower in constrictive pericarditis than in restrictive cardiomyopathy. The %E for peak diastolic flow was larger in constrictive pericarditis (29% vs. 16%, p = 0.008). The pulmonary venous systolic/diastolic flow ratio was greater in constrictive pericarditis in both inspiration and expiration. The combination of pulmonary venous systolic/diastolic flow ratio > or = 0.65 in inspiration and a %E for peak diastolic flow > or = 40% correctly classified 86% of patients with constrictive pericarditis. CONCLUSIONS: The relatively larger pulmonary venous systolic/diastolic flow ratio and greater respiratory variation in pulmonary venous systolic, and especially diastolic, flow velocities by transesophageal echocardiography can be useful signs in distinguishing constrictive pericarditis from restrictive cardiomyopathy.

Blood Flow Velocity↗
PubMed1993

Reversal of volatile anesthetic-induced depression of myocardial contractility by extracellular calcium also enhances left ventricular diastolic function.

BACKGROUND: Volatile anesthetics depress global left ventricular function by altering intracellular calcium (Ca2+) homeostasis at several sites within the myocyte. Although extracellular Ca2+ partially reverses the negative inotropic effects of volatile anesthetics, the actions of extracellular Ca2+ on anesthetic-induced diastolic dysfunction are unexplored. This investigation examined and compared the direct effects of extracellular Ca2+ on left ventricular systolic and diastolic function in conscious and anesthetized dogs. METHODS: Experiments were conducted in the presence of pharmacologic blockade of the autonomic nervous system because autonomic nervous activity may significantly influence the hemodynamic actions of anesthetics and Ca2+ in vivo. Three groups comprised a total of 27 experiments conducted using nine dogs chronically instrumented for measurement of aortic and left ventricular pressure, left ventricular dP/dt, subendocardial segment length, and cardiac output. Myocardial contractility was evaluated using the preload recruitable stroke work relationship slope (Mw). Diastolic function was assessed using a time constant of isovolumic relaxation (tau), a regional chamber stiffness constant (Kp), and maximum segment lengthening velocity during rapid ventricular filling (dL/dtE) and atrial systole (dL/dtA). On 3 separate days, a CaCl2 infusion at 1.25, 2.5, or 5 mg.kg-1 x min-1 was administered. Hemodynamics and ventricular pressure-length loops were recorded after a 20-min equilibration at each dose in the conscious state or during halothane or isoflurane anesthesia. RESULTS: In conscious dogs, CaCl2 produced a significant (P < .05) and dose-dependent increase in contractility as evaluated by Mw. In the presence of halothane anesthesia, CaCl2 increased contractility (Mw of 26 +/- 5 mmHg to 78 +/- 10 mmHg during the high dose of CaCl2), enhanced isovolumic relaxation (tau of 57.9 +/- 4.2 ms to 41.1 +/- 1.9 ms during the high dose of CaCl2), improved rapid ventricular filling (dL/dtE of 11.8 +/- 1.4 mm/s to 20.2 +/- 1.6 mm/s during the high dose of CaCl2), and reduced regional chamber stiffness (Kp of 0.70 +/- 0.18 mm-1 to 0.38 +/- 0.04 mm-1 during the high dose of CaCl2). Similar findings were observed when CaCl2 was administered to dogs anesthetized with isoflurane. CONCLUSIONS: Although CaCl2 produced positive inotropic effects in both the conscious and anesthetized states, CaCl2 did not alter diastolic function in conscious dogs. In contrast, CaCl2 reversed halothane- and isoflurane-induced negative lusitropic actions. The results of the present investigation suggest that improvement of left ventricular performance by CaCl2 during volatile anesthesia may be related to actions in diastole as well as systole.

Anesthesia, Inhalation↗
PubMed2004

Genetic manipulation of calcium-handling proteins in cardiac myocytes. II. Mathematical modeling studies.

We developed a mathematical model specific to rat ventricular myocytes that includes electrophysiological representation, ionic homeostasis, force production, and sarcomere movement. We used this model to interpret, analyze, and compare two genetic manipulations that have been shown to increase myocyte relaxation rates, parvalbumin (Parv) de novo expression, and sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA2a) overexpression. The model was used to seek mechanistic insights into 1) the relative contribution of two mechanisms by which SERCA2a overexpression modifies Ca2+ sequestration, i.e., more pumps and an increase in the SERCA2a-to-phospholamban ratio, 2) the mechanisms behind postrest potentiation and how Parv and SERCA2a influence this response, and 3) why Parv myocytes retain their fast kinetics when endogenous SERCA2a is partially impaired by thapsigargin (a condition used to mimic diastolic dysfunction). The model was also utilized to predict whether Parv metal-binding characteristics might be modified to improve diastolic and systolic functions and whether Parv or SERCA2a might affect diastolic Ca2+ levels and myocyte energetics. One outcome of the model was to demonstrate a higher peak and total ATP consumption in SERCA2a myocytes and more even distribution of ATP throughout the cardiac cycle in Parv myocytes. This may have implications for failing hearts that are energetically compromised.

Animals↗
PubMed2003

Impact of acute hypoxic pulmonary hypertension on LV diastolic function in healthy mountaineers at high altitude.

In pulmonary hypertension right ventricular pressure overload leads to abnormal left ventricular (LV) diastolic function. Acute high-altitude exposure is associated with hypoxia-induced elevation of pulmonary artery pressure particularly in the setting of high-altitude pulmonary edema. Tissue Doppler imaging (TDI) allows assessment of LV diastolic function by direct measurements of myocardial velocities independently of cardiac preload. We hypothesized that in healthy mountaineers, hypoxia-induced pulmonary artery hypertension at high altitude is quantitatively related to LV diastolic function as assessed by conventional and TDI Doppler methods. Forty-one healthy subjects (30 men and 11 women; mean age 41 +/- 12 yr) underwent transthoracic echocardiography at low altitude (550 m) and after a rapid ascent to high altitude (4,559 m). Measurements included the right ventricular to right atrial pressure gradient (DeltaP(RV-RA)), transmitral early (E) and late (A) diastolic flow velocities and mitral annular early (E(m)) and late (A(m)) diastolic velocities obtained by TDI at four locations: septal, inferior, lateral, and anterior. At a high altitude, DeltaP(RV-RA) increased from 16 +/- 7 to 44 +/- 15 mmHg (P < 0.0001), whereas the transmitral E-to-A ratio (E/A ratio) was significantly lower (1.11 +/- 0.27 vs. 1.41 +/- 0.35; P < 0.0001) due to a significant increase of A from 52 +/- 15 to 65 +/- 16 cm/s (P = 0.0001). DeltaP(RV-RA) and transmitral E/A ratio were inversely correlated (r(2) = 0.16; P = 0.0002) for the whole spectrum of measured values (low and high altitude). Diastolic mitral annular motion interrogation showed similar findings for spatially averaged (four locations) as well as for the inferior and septal locations: A(m) increased from low to high altitude (all P < 0.01); consequently, E(m)/A(m) ratio was lower at high versus low altitude (all P < 0.01). These intraindividual changes were reflected interindividually by an inverse correlation between DeltaP(RV-RA) and E(m)/A(m) (all P < 0.006) and a positive association between DeltaP(RV-RA) and A(m) (all P < 0.0009). In conclusion, high-altitude exposure led to a two- to threefold increase in pulmonary artery pressure in healthy mountaineers. This acute increase in pulmonary artery pressure led to a change in LV diastolic function that was directly correlated with the severity of pulmonary hypertension. However, in contrast to patients suffering from some form of cardiopulmonary disease and pulmonary hypertension, in these healthy subjects, overt LV diastolic dysfunction was not observed because it was prevented by augmented atrial contraction. We propose the new concept of compensated diastolic (dys)function.

Acute Disease↗
PubMed1990

[The assessment of left ventricular diastolic function in patients with aortic defects].

Thirty patients with aortic heart disease and 10 healthy persons were examined for diastolic function of the left ventricle using two-dimensional Doppler echocardiography. The decline of the rate and volume of early diastolic filling, the rise of the filling during the atrial systole were revealed in 60% of the patients with aortal disease. The decrease of the ejection fraction of the left ventricle was noted in 23.3% of the patients. All the patients with aortic disease were distributed into 2 groups depending on the presence (group II) or lack (group I) of mitral regurgitation. Addition of mitral regurgitation in patients with aortic disease masked the deranged filling of the left ventricle and interfered with the diagnosis of diastolic dysfunction. A reverse moderately pronounced relationship (r = -0.56) has been discovered between the myocardial mass and impairment of the diastolic filling.

Adult↗
PubMed2003

Improving outcomes in diastolic heart failure. Techniques to evaluate underlying causes and target therapy.

Abnormal diastolic function is a common cause of clinical heart failure, particularly among elderly patients. Through early diagnosis and careful management of diastolic dysfunction, these patients can expect improved functional capacity and, in some cases, a favorable long-term outcome. In this article, Drs Torosoff and Philbin discuss how to confirm the diagnosis of diastolic heart failure through objective testing. Current approaches to the treatment of symptoms, including reduction of intravascular volume, heart rate control, and elimination of precipitating factors, are also presented.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Left ventricular restoring forces: modulation by heart rate and contractility.

We used a servomotor system in open-chest dogs to rapidly clamp left atrial pressure below left ventricular (LV) diastolic pressure in order to produce nonfilling diastoles during which the LV fully relaxed at its end-systolic volume (ESV). Restoring forces (RFs) generated during contraction which result in LV filling by suction were considered to be present when the fully relaxed pressure (FRP) was negative. We characterized RFs in terms of the fully relaxed pressure-volume relation (FRPV relation, FRP plotted vs ESV), which has negative and positive portions and an equilibrium volume (FRP = 0 mmHg). A negative FRP is ordinarily present over the lower half of the physiologic filling range. Increased contractility (systemic dobutamine) shifts the FRPV relation downward, indicating greater RFs at any ESV. Intracoronary dobutamine administered via the left anterior descending coronary artery has the same effect. Acute increases in heart rate from about 100 to 150 beats/min did not alter the FRPV relation. In contrast, chronic tachycardia heart failure resulted in marked depression of the ability to generate RFs, even at very low volumes. Thus, RFs normally contribute to LV filling. They are augmented by acute increases in global and anterior wall contractility but not heart rate, within the range specified above. Chronic tachycardia heart failure markedly attenuated RFs. The latter may constitute a previously unappreciated mechanism of diastolic dysfunction in heart failure.

Animals↗
PubMed2006

[Is the left ventricle enddiastolic pressure pathological in the older population?].

INTRODUCTION: The percentage of older population has significantly increased in the recent decades. Morphologic and functional changes of the cardiovascular system go together with ageing. The aim of the study should show the correlation between the age and left ventricular enddiastolic pressure (LVDEP) value. METHODS: 106 patients of the age from 23 to 79 years without an organic heart disease and the history of hypertension underwent elective coronary angiography including left ventricle angiography between 1999 and 2002. LVEDP was obtained as an average value from 8 consecutive beats without extrasystoles. According to the relation between increased relative frequency of LVEDP and age patients were divided into two groups: 50 years and older (80 patients) and younger than 50 years (26 patients). RESULTS: An average LVEDP value in older population versus younger population was 12.1 +/- 5.0 mm Hg vs 8.9 +/- 3.4 mm Hg, p < 0.05. Increased LVEDP in yonger population was found in only 11.5 % vs 46.2 % in older group, p < 0.01 and the LVEDP was age dependent, p < 0.05. CONCLUSIONS: In compliance with about mentioned results we suppose that the age is a factor with impact to LVEDP value. LVEDP values > 12 mm Hg in older population may not be pathological and probably are due to the left ventricle diastolic dysfunction in consequence with ageing.

Adult↗
PubMed1995

Prevalence, clinical features and prognosis of diastolic heart failure: an epidemiologic perspective.

Numerous reports suggest that about one-third of patients with congestive heart failure do not have any abnormality of left ventricular systolic function. These patients presumably have heart failure on the basis of ventricular diastolic dysfunction. Our objective was to develop a comprehensive overview of published reports of the prevalence, clinical features and prognosis of diastolic heart failure and to offer recommendations for future studies. Thirty-one studies of patients with congestive heart failure with normal left ventricular systolic function were published in the time period from January 1970 through March 1995. These studies were identified with the use of computer-based searches in relevant data bases. Among patients with congestive heart failure, the prevalence of normal ventricular systolic performance in the published reports varies widely from 13% to 74%; the reported annual mortality rate also varies from 1.3% to 17.5%. The criteria for congestive heart failure, its chronicity and the age of the study sample affect the reported prevalence and prognosis of the disorder. The clinical signs and symptoms of diastolic heart failure are similar to those of patients with systolic heart failure, underscoring the need for evaluation of ventricular systolic function in patients with congestive heart failure. In the absence of any large-scale randomized clinical trial targeting these patients, the optimal treatment of diastolic heart failure is unclear. We conclude that the heterogeneity in previous studies of diastolic heart failure hinders the comparison of published reports. There is a need to conduct prospective, community-based investigations to better characterize the incidence, prevalence and natural history of diastolic heart failure. Randomized clinical trials are needed to determine optimal treatment strategies.

Diastole↗
PubMed2006

Hypothyroidism leads to increased collagen-based stiffness and re-expression of large cardiac titin isoforms with high compliance.

Because long-term hypothyroidism results in diastolic dysfunction, we investigated myocardial passive stiffness in hypothyroidism and focused on the possible role of titin, an important determinant of diastolic stiffness. A rat model of hypothyroidism was used, obtained by administering propylthiouracil (PTU) for times that varied from 1 month (short-term) to 4 months (long-term). Titin expression was determined by transcript analysis, gel electrophoresis and immunoelectron microscopy. Diastolic function was measured at the isolated heart, skinned muscle, and cardiac myocyte levels. We found that hypothyroidism resulted in expression of a large titin isoform, the abundance of which gradually increased with time to become the most dominant isoform in long-term hypothyroid rats. This isoform co-migrates on high-resolution gels with fetal cardiac titin. Transcript analysis on myocardium of long-term PTU rats, provided evidence for expression of additional PEVK and Ig domain exons, similar to what has been described in fetal myocardium. Consistent with the expression of a large titin isoform, titin-based restoring and passive forces were significantly reduced in single cardiac myocytes and muscle strips of long-term hypothyroid rats. Overall muscle stiffness and LV diastolic wall stiffness were increased, however, due to increased collagen-based stiffness. We conclude that long term hypothyroidism triggers expression of a large cardiac titin isoform and that the ensuing reduction in titin-based passive stiffness functions as a compensatory mechanism to reduce LV wall stiffness.

Animals↗
PubMed2003

Chronic inappropriate sinus tachycardia in elderly females.

BACKGROUND: The vast majority of reports of inappropriate sinus tachycardia (IST) had included predominantly young females with ages ranging between 15 and 46 years. In contrast, the present study presents the findings in four elderly females (aged 61-71 years) with long-standing symptoms of palpitations, more than 15 years, in whom IST was diagnosed in their 6th or 7th decade. METHODS: Clinical and laboratory examinations including electrocardiograms, echocardiograms, and heart rate variability studies were retrospectively reviewed in four of the nine elderly female patients with long-standing cardiac symptoms. Indices of heart rate variability were compared to four age-matched asymptomatic elderly females with no structural heart disease. RESULTS: The resting electrocardiograms were normal but one had voltage criteria for left ventricular hypertrophy. All traditional time- and frequency-domain indices were significantly decreased in the symptomatic elderly females as compared to the controls. Echocardiograms showed normal ejection fraction, and in three patients evidence of diastolic dysfunction and mild left ventricular hypertrophy. Blood pressures were elevated, with systolic blood pressure ranging from 170 to 190 and diastolic blood pressure ranging from 94 to 106. Anxiety disorders were diagnosed in all patients. CONCLUSIONS: This study demonstrates that IST can be present in a wide spectrum of patient populations, including elderly populations. It seems that some cases of IST can become chronic if not treated adequately. Apparently, earlier identification and treatment could have improved the quality of life of the patients. Traditional HRV indices may not be valuable to support either a sympathetic or parasympathetic mechanism. Therefore, further studies should consider the potential usefulness of the nonlinear method such as, for example, approximate entropy and detrended fluctuation analysis.

Aged↗
PubMed2006

Evaluation of asymptomatic patients with chronic Chagas disease through ambulatory electrocardiogram, echocardiogram and B-Type natriuretic peptide analyses.

OBJECTIVE: To evaluate asymptomatic patients with chronic Chagas disease to determine prevalence of ventricular arrhythmias, left ventricular dysfunction, and B-type natriuretic peptide (BNP) plasma levels. METHODS: One hundred and six patients from the Chagas disease outpatient clinic underwent clinical evaluation, electrocardiogram (ECG), cardiothoracic index (CTI), ambulatory electrocardiogram (Holter monitoring), echocardiogram, and BNP measurement and then were distributed into three groups: GI, with normal ECG (n = 50); GIIA, with ECG changes characteristic of Chagas disease (n = 31); and GIIB, with other ECG changes (n = 25). RESULTS: The most common electrocardiographic changes were the following. GIIA: complete right bundle branch block (35%), left anterior hemiblock (35%), and electrically inactive areas (32%); GIIB: inferolateral repolarization change (28%), and left ventricular overload (24%). Mean CTI index values were similar (p = 0.383). Ventricular arrhythmia prevalence was higher in the GIIA (77%) and GIIB (75%) groups than in the GI group (46%) (p = 0.002). Ventricular dysfunction was more prevalent in the GIIA (52%) and GIIB (32%) groups than in the GI group (14%) (p = 0.001). Systolic dysfunction was more prevalent in the GIIA group (29%) than in the GIIB (20%) and GI groups (2%) (p < 0.001). Diastolic dysfunction was more prevalent in the GIIA (42%) and GIIB (28%) groups than in the GI group (12%) (p = 0.005). Mean B-type natriuretic peptide levels were 30 +/- 88 pg/mL in the GI group, 66 +/- 194 in the GIIA group and 24 +/- 82 for the GIIB group (p = 0.121), respectively. CONCLUSION: Arrhythmias and left ventricular dysfunction are more prevalent in asymptomatic patients with chronic Chagas disease and abnormal ECG than in patients with normal ECG. Plasma BNP levels were similar among the groups.

Adult↗
PubMed2004

[Diabetes mellitus, left ventricular dysfunction and congestive heart failure].

Diabetes is a well known risk factor for the development of congestive heart failure. Epidemiological evidence in the community underscores the prevalence of left ventricular systolic dysfunction in diabetic patients as 2-fold with respect to non-diabetic ones, with half of them completely asymptomatic. Diastolic dysfunction in diabetic hearts, in comparison with non-diabetic, is even more frequent. The high prevalence has been explained by the frequent coexistence of an underlying diabetic cardiomyopathy, hypertension and ischemic heart disease. In these patients, the diabetic metabolic derangement, together with the early activation of sympathetic nervous system, induce a decrease of myocardial function. The activation of renin-angiotensin system results in an unfavorable cardiac remodeling. The progression from myocardial damage to overt dysfunction and heart failure is often asymptomatic for a long time and frequently undiagnosed and untreated. Currently, the widespread availability of echocardiography and possibly the use of cardiac natriuretic peptides, may allow for an earlier recognition of most of such patients. In heart failure, diabetic patients have a worse prognosis than non-diabetics. The available pharmacological treatments, such as ACE-inhibitors, beta-blockers and possibly angiotensin receptor blockers, togheter with a tight glycemic control, may be effective to reverse the remodeling process and prevent cardiovascular events. In order to identify most of the diabetic patients at risk of development of left ventricular dysfunction and to prevent its progression to overt heart failure, it seems important to elaborate a screening strategy in order to diagnose and treat most of diabetic patients with myocardial damage.

Diabetes Complications↗
PubMed1995

Potential mechanisms of improvement after various treatments for hypertrophic obstructive cardiomyopathy.

In sum, systolic dysfunction of the ventricle associated with left ventricular outlet obstruction and often with mitral valve regurgitation may be improved by myotomy, myomectomy, mitral valve replacement, and perhaps by the creation of left bundle branch block via DDD right ventricular pacing. Diastolic dysfunction of the ventricle may be improved by prolonging the diastolic filling period, shortening the isovolumic relaxation period with calcium channel blocking drugs, or perhaps by altering the atrioventricular activation time with a DDD pacemaker. The symptoms and complications of associated arrhythmias may be improved by medication, particularly with beta-blockers, which tend to stabilize the atrial rhythm and perhaps the ventricular rhythms. In treating patients with demonstrated ventricular arrhythmias, other antiarrhythmic agents may be helpful. (Table II summarizes the abnormalities, causes, and treatments of hypertrophic obstructive cardiomyopathy.) Epicardial coronary atherosclerosis is not rare in these patients, and arteriographic confirmation may lead to improvement by surgical bypass treatment. Since stroke volume is nearly fixed, cardiac output depends very much on heart rate. For this reason, each patient needs to receive the appropriate dosage of medications to achieve the optimal heart rate for his or her own physiologic state.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Tissue Doppler imaging and gradient echo cardiac magnetic resonance imaging in normal cats and cats with hypertrophic cardiomyopathy.

Cats with hypertrophic cardiomyopathy (HCM) often develop diastolic dysfunction, which can lead to development of left congestive heart failure. Tissue Doppler imaging (TDI) echocardiography has emerged as a useful, noninvasive method for assessing diastolic function in cats. Cardiac magnetic resonance imaging (cMRI) has been performed in cats and accurately quantifies left ventricular (LV) mass in normal cats. However, assessment of cardiac function in cats by cMRI has not been performed. Six normal Domestic Shorthair cats and 7 Maine Coon cats with moderate to severe HCM were sedated, and TDI of the lateral mitral annulus was performed. Peak early diastolic velocity (Em) was measured from 5 nonconsecutive beats. Cats were anesthetized with propofol and electrocardiogram-gated gradient echo cMRI was performed during apnea after hyperventilation. Short-axis images of the LV extending from the mitral annulus to the apex were obtained throughout the cardiac cycle. LV mass at end systole and LV volumes throughout the cardiac cycle were quantified according to Simpson's rule. To assess the possible influence of propofol on diastolic function, TDI was performed on the 7 cats with HCM while sedated and then while anesthetized with propofol. Em was significantly lower in cats with HCM than normal cats (6.7 +/- 1.3 cm/s versus 11.6 +/- 1.9 cm/s, P < .001, respectively). There was no difference in the cMRI indices of diastolic function in normal and HCM cats. Propofol did not reduce diastolic function (Em) in cats with HCM but mildly reduced systolic myocardial velocity (S) in Maine Coon cats with HCM that were anesthetized with propofol (P = .87 and P = .03, respectively).

Animals↗
PubMedDate not supplied

Prophylactic effects of an N- and L-type Ca2+ antagonist, cilnidipine, against cardiac hypertrophy and dysfunction in stroke-prone, spontaneously hypertensive rats.

To clarify the beneficial effects of cilnidipine, an L- and N-type calcium channel blocker, which were clinically observed against diastolic dysfunction in hypertrophied hearts of hypertensive patients, we investigated the effects of cilnidipine on cardiac remodeling and enhanced gene expression in stroke-prone, spontaneously hypertensive rats in comparison with that of captopril, a well-known angiotensin-converting enzyme inhibitor, at threshold doses with little blood pressure lowering effect. The expression of type III collagen and beta/alpha-myosin heavy chain as well as transforming growth factor-beta, and basic fibroblast growth factor were suppressed by both treatments, indicating the prevention or amelioration of cardiac dysfunction. Such beneficial effects were much more intense with cilnidipine treatment than in captopril. These results indicate that Ca2+ is a key factor in the pathogenesis of cardiac remodeling in hypertension. One possible beneficial effect of cilnidipine in the prevention of cardiac dysfunction may be due to the decreased amount of growth factors such as transforming growth factor-beta and basic fibroblast growth factor via direct action for Ca2+ influx and also via inhibition of local renin-angiotensin system in the myocardium.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Usefulness of Doppler myocardial imaging for identification of mutation carriers of familial hypertrophic cardiomyopathy.

Because myocyte dysfunction and disarray are early abnormalities in hypertrophic cardiomyopathy (HC), we tested if Doppler myocardial imaging (DMI) could identify systolic and diastolic dysfunction in mutation carriers (MC) (genotype positive patients without hypertrophy, defined as phenotype negative after conventional screening tests). In a single family with a missense mutation in the myosin binding protein C gene (Arg 502 Gln) we identified 5 MCs; these subjects were asymptomatic and had normal physical examination, normal electrocardiogram, treadmill stress test, ambulatory Holter electrocardiogram, and normal conventional M-mode, 2-dimensional, and Doppler echocardiography. In each patient we performed a DMI study and measured the peak velocities of the systolic (S), rapid filling (E), and atrial contraction (A) waves in the 4 sides of the mitral annulus, in 8 left ventricular segments (apical views), in the tricuspid annulus, and in 2 right ventricular segments. These data were compared with those from 10 normal volunteers matched for sex, age, and body surface. Compared with the normal volunteers, the MCs had lower left ventricular systolic velocities and higher right ventricular systolic velocities; lower diastolic rapid filling velocities; higher or similar atrial contraction velocities; reduced E/A; lower percentage of annular sides and segments with E/A >1 and lower average number of sides and/or segments with E/A >1 per patient; similar right ventricular rapid filling velocities; and similar or higher atrial contraction wave velocities. Thus, DMI detects important left and right ventricular annular and regional myocardial contraction and relaxation abnormalities independently of the presence of hypertrophy, in HC. These results show that DMI is more sensitive than conventional echocardiography and establishes a new and highly accurate method for the noninvasive screening of MCs of the disease.

Adult↗