Secondary Left Ventricular Hypertrophy Research Articles

Abstract 4139187: Electrophysiological and Mechanical Characterization of Human Ventricular Myocardium from Patients with Primary or Secondary Cardiac Hypertrophy

Left-ventricular hypertrophy (LVH) is an adaptive condition to hemodynamic stress often involving the left ventricle (LV). This pathological condition is associated with clinical complications such as ventricular arrhythmias and diastolic dysfunction, the molecular and cellular mechanisms of which have been poorly investigated in the human heart. We collected myocardial samples from the upper interventricular septum of 132 patients with hypertrophic cardiomyopathy (HCM), 42 patients with aortic stenosis and severe LVH (AoS-LVH) and 12 non-failing non-hypertrophic patients with valve disease (NF-NH), who underwent myectomy operations at our cardiac surgery center. Samples were used to isolate single viable cardiomyocytes from the left ventricle to perform patch-clamp electrophysiological studies and intracellular calcium measurements with fluorescent dyes. Intact trabeculae were also dissected to perform isometric force measurements of electrically-stimulated twitches. Single-cell patch-clamp studies revealed a marked prolongation of action potential duration (APD) in HCM (N=82, mean APD at 90% repolarization=763±252ms at 0.5Hz) and AoS-LVH (N=22, APD90%=579±147ms) samples with respect to NF-NH (N=12, APD90%=447±88ms). In both HCM and AoS-LVH cardiomyocytes, APD prolongation was associated with increased late-Na + current with respect to NF-NH, while L-type Ca 2+ current was enlarged only in HCM samples. Ca 2+ -fluorescence studies revealed markedly slower Ca-transient (CaT) kinetics in myocardial samples from HCM (N=38, mean CaT 50% decay time at 0.5 Hz = 658±179ms) and AoS-LVH patients (N=9, CaT50%= 568±187ms), when compared with NF-NH samples (N=8, CaT50%=283±59ms), paralleled by elevated diastolic [Ca 2+ ]. Twitch force measurements in intact trabeculae revealed prolonged isometric contractions in HCM (N=78, overall twitch duration at 0.5Hz= 730±147ms) and in AoS-LVH patient-samples (N=24, TwD=669±116ms), as compared with NF-NH (N=7, TwD=511±73ms). Force-frequency relationship was flat in pathological samples, while NF-NH trabeculae showed a clear increase in twitch amplitude while increasing pacing rate to 2Hz. Our results suggest that the main features of functional cardiomyocyte remodeling (that is, changes in the expression and/or function of ion-channel and EC-coupling proteins) are qualitatively similar in primary vs. secondary LVH, albeit abnormalities are quantitatively more extensive in HCM samples.

РЕЗУЛЬТАТЫ ЭЛЕКТРОКАРДИОГРАФИЧЕСКОГО ИССЛЕДОВАНИЯ ПРИ ГКМП У РАЗНОВОЗРАСТНЫХ КОШЕК

Cardiomyopathies are a heterogeneous group of myocardial diseases with varying phenotypes and prognosis. Feline cardiomyopathies are common, and cardiovascular disease is among the 10 most common causes of death in cats. Hypertrophic cardiomyopathy (HCM) is a common cause of heart failure, arterial thromboembolism, and sudden death in cats. HCM is a primary myocardial lesion characterized by unexplained left ventricular hypertrophy (LVH) and impaired myocardial relaxation. The cause of primary or idiopathic in cats is unknown, but hereditary pathology probably exists in many cases. The disease is widespread in breeds such as Maine Coon, Persian, Ragdoll, American Shorthair. There are also reports of HCM in littermates and other close relatives of domestic shorthair cats. The method of electrocardiography is quite sensitive in the diagnosis of cardiomyopathies in humans, therefore, the study of ECG signs of HCM in cats, as well as the study of the dynamics of disease progression, the development and improvement of the treatment of this disease is an urgent scientific and practical problem in veterinary medicine, which has not been sufficiently resolved to date. According to the obtained ECG data, it can be concluded that recording in animals of different ages, as well as in animals that have a hereditary predisposition to the development of this disease, can play a key role in diagnosing an early stage of cardiomyopathy. The prevalence of HCM in cats with a predisposition to this disease is much higher than in cats without this genetic predisposition. Further studies involving more cats with HCM, secondary left ventricular hypertrophy, and normal hearts are proposed to better understand the heterogeneity and complexity of this myocardial disease.

Echocardiographic strain in hypertrophic cardiomyopathy and hypertensive left ventricular hypertrophy.

The myocardial structure differs between secondary left ventricular hypertrophy (LVH) and hypertrophic cardiomyopathy (HCM). We investigated left ventricular function of these two types of hypertrophy using multilayer strain analysis with two-dimensional echocardiography. Transthoracic echocardiography (Vivid-E9) was performed in 240 patients with preserved left ventricular ejection fraction (LVEF ≥50%) and with either HCM (n=80, 63 men, age 49.8±14.1years), hypertensive LVH (n=80, 63 men, age 51.4±13.3years) or normal blood pressure and left ventricular structure (n=80, 63 men, 50.8±12.4years). Quantitative multilayer longitudinal strain (LS), circumferential strain (CS), and radial strain (RS) were analyzed. The ratio of endo-/epi-myocardial strain was calculated. Longitudinal strain was significantly (P<0.001) lower in HCM patients than normal controls (15.2±4.2% vs 23.1±2.7%), especially in hypertrophic segments (14.5±4.4% vs 17.2±3.2% in nonhypertrophic segments, P<0.01). LS was lower in patients with hypertensive LVH, similarly in all left ventricular segments (20.7±3.7%, P<0.001 vs controls). CS was lower in the mid- and epicardium (P<0.01), but not endocardium in HCM (P=0.4), and preserved in all myocardial layers in hypertensive LVH. The endo-/epi-myocardial ratios of both LS and CS were higher in HCM than hypertensive LVH (P<0.01). RS was higher (P<0.01) in HCM than hypertensive LVH and controls. Endocardial CS and global RS were correlated with LVEF (r≥0.32, P<0.01). Hypertrophic cardiomyopathy patients had marked reductions in LS and CS, whereas patients with hypertensive LVH had less reduction in LS and preserved CS. The increased endo-/epi-myocardial ratios of LS and CS may be useful in differentiating HCM from hypertensive LVH.

Clinical characteristics and outcome of hypertrophic cardiomyopathy in the Saudi population – A single cardiac center experience

Introduction Hypertrophic Cardiomyopathy (HCM), a relatively uncommon entity, is the most common form of genetic cardiovascular disorders. It is the most common cause of sudden death in the young and also heart failure which can occur at any age. While HCM is a well-described global disorder, there is paucity of data on this important clinical entity in Saudi Arabia. Therefore, the aim of this study was to explore the clinical characteristics and outcome of HCM in a Saudi population attending King Abdul Aziz Cardiac Center (KACC), Riyadh. Methodology We retrospectively collected electronic echocardiographic data in adult HCM patients at KACC, Riyadh, between January 1st 2002 and December 31st 2016 (Xcelera™). Cases of secondary left ventricular hypertrophy were excluded. In addition, demographic, anthropometric, comorbidities and outcome data was also recorded (Apollo Lx). Data was analysed using JMP version 7.1 (SAS for Windows). Results Data were available for 77 patients, mean age 40 ± 17 years, 63.6% males. Commonest comorbidities included hypertensive (23.5%), diabetes mellitus (15.6%), coronary artery disease (15.6%) stroke (10.4%), atrial fibrillation (13 %) and ventricular tachycardia (5%). Half of the population had associated mitral regurgitation. Nine percent of patients had a history of syncope and 13% family history of sudden cardiac death. There was a significant interaction between age and HCM morphology (p Conclusion The HCM population in our Center is young, predominantly male with largely reverse curvatum morphology and mitral regurgitation observed in half of the cases. A country-wide registry is warranted to further explore HCM phenotypes in the Saudi population.

Left ventricular hypertrophy or storage disease? the incremental value of speckle tracking strain bull's-eye.

Left ventricular hypertrophy (LVH) develops in response to a variety of physical, genetic, and biochemical stimuli and represents the early stage of ventricular remodeling. In patients with LVH, subclinical left ventricular (LV) dysfunction despite normal ejection fraction (EF) may be present before the onset of symptoms, which portends a dismal prognosis. Strain measurement with two-dimensional speckle tracking echocardiography (STE) represents a highly reproducible and accurate alternative to LVEF determination. The present review focuses on current available evidence that supports the incremental value of STE in the diagnostic and prognostic workup of LVH. When assessing the components of LV contraction, STE has an incremental value in differentiating between primary and secondary LVH and in the differential diagnosis with storage diseases. In addition, STE provides unique information for the stratification of patients with LVH, enabling to detect intrinsic myocardial dysfunction before LVEF reduction.

Sténose aortique et lésions coronaires : la fractional flow reserve (FFR) est-elle valide ?

A 54-year-old woman was hospitalized for an acute pulmonary oedema revealing a severe aortic stenosis (AS) associated with an aortic aneurysm and a left ventricular hypertrophy (LVH). The coronary angiography found an equivocal left main lesion. Fractional flow reserve (FFR) showed hemodynamic significance (FFR=0.78) and optical coherence tomography confirmed this result with a minimal lumen area of 4.9mm2. FFR-guided percutaneous intervention is reported to improve outcome in patients with stable coronary disease. However, only few data are available in cases of AS. In this condition, secondary LVH is associated with microcirculatory dysfunction, which interferes with optimal hyperemia. An elevated right atrial pressure could also modify FFR measurement. This risk of underestimation of a coronary lesion in patients with severe AS has to be taken into consideration in clinical practice.

A stumbling block or a stepping stone?

Question A 60-year-old man, known with Fabry disease, secondary left ventricular hypertrophy, and moderate aortic valve stenosis had a check-up in the outpatient clinic. An electrocardiogram (ECG) at rest (Fig. 1) showed sinus rhythm, a short PR interval, QRS interval of 120 ms with a sharp initial part suggestive of pre-excitation, as well as other unchanged abnormalities, including signs of left ventricular hypertrophy. In order to examine this possible pre-excitation suggestive of a right-sided, septal bypass an exercise test was performed. Unfortunately, the test was stopped after only 2 min due to exhaustion with a maximal heart rate of only 83/minute, without changes in QRS morphology. Because of a negative history of collapse or palpitations no further diagnostic tests were performed. Four months later, he was admitted because of a collapse. The ECG at presentation is shown in Fig. 2. Fig. 1 ECG at rest Fig. 2 ECG in the emergency room What is your diagnosis, and what does it tell you about the possible pre-excitation? Answer You will find the answer elsewhere in this issue.

Systemic Hypertension in Patients with Aortic Stenosis: Clinical Implications and Principles of Pharmacological Therapy.

The treatment of systemic hypertension (HTN) in patients with Aortic stenosis (AS) requires a careful balance of lowering the systemic blood pressure without compromising vital organ perfusion and worsening of the symptoms of AS. Treatment of systemic HTN is beneficial because the combination of HTN and AS provides additional overload to the left ventricle. This leads to secondary Left ventricular hypertrophy (LVH), which has been shown to increase cardiovascular risks and mortality and thus early presentation of symptoms of AS. Additionally, presence of HTN may affect the accurate assessment of AS. Different treatment options are available, however no specific treatment guidelines have been established for patients with concomitant AS and HTN. Improved control of HTN is the key to prevent symptom progression and inadvertent early surgery. Angiotensin converting enzyme inhibitors (ACEi) and Angiotensin receptor blockers (ARB) appear to be beneficial. Reassessment of the aortic valve by echocardiography is recommended after HTN is well controlled before deciding on aortic valve replacement (AVR).

TAVI and Left Ventricular Hypertrophy - A Case Report

Introduction: Severe aortic valve stenosis in elderly patients is often accompanied by secondary left ventricular hypertrophy due to chronic pressure overload. Transaortic valve intervention is a valuable technique in high-risk patients, however in case of extensive left ventricular outflow tract obstruction surgery including enlargement of the left ventricular outflow tract (LVOT) may be indicated.

Results of catheter ablation of atrial fibrillation in hypertrophied hearts – Comparison between primary and secondary hypertrophy

Background and purposeApproximately 20–25% of the patients with hypertrophic cardiomyopathy (HCM) develop atrial fibrillation (AF) during the clinical course of the disease, a percentage significantly larger than that of the general population. The purpose of the present study was to report on the procedural results of patients with AF and either primary or secondary left ventricular hypertrophy (LVH). Methods and subjectsTwenty-two consecutive HCM patients (55% male, mean age 57±8 years) with symptomatic AF, having undergone AF ablation procedures between September 2009 and July 2012 were compared with respect to procedural outcome and follow-up characteristics with 22 matched controls with secondary cardiac hypertrophy (64% male, 63±10 years) from our prospective AF catheter ablation registry. Results and conclusionRadiofrequency catheter ablation (RFCA) was successful in restoring long-term sinus rhythm in patients with LVH due to HCM and due to secondary etiology. However, patients with HCM needed more RFCA procedures and frequently additional antiarrhythmic drug therapy in order to maintain sinus rhythm.

Mutations in MYH7 reduce the force generating capacity of sarcomeres in human familial hypertrophic cardiomyopathy

Familial hypertrophic cardiomyopathy (HCM), frequently caused by sarcomeric gene mutations, is characterized by cellular dysfunction and asymmetric left-ventricular (LV) hypertrophy. We studied whether cellular dysfunction is due to an intrinsic sarcomere defect or cardiomyocyte remodelling. Cardiac samples from 43 sarcomere mutation-positive patients (HCMmut: mutations in thick (MYBPC3, MYH7) and thin (TPM1, TNNI3, TNNT2) myofilament genes) were compared with 14 sarcomere mutation-negative patients (HCMsmn), eight patients with secondary LV hypertrophy due to aortic stenosis (LVHao) and 13 donors. Force measurements in single membrane-permeabilized cardiomyocytes revealed significantly lower maximal force generating capacity (Fmax) in HCMmut (21 ± 1 kN/m²) and HCMsmn (26 ± 3 kN/m²) compared with donor (36 ± 2 kN/m²). Cardiomyocyte remodelling was more severe in HCMmut compared with HCMsmn based on significantly lower myofibril density (49 ± 2 vs. 63 ± 5%) and significantly higher cardiomyocyte area (915 ± 15 vs. 612 ± 11 μm²). Low Fmax in MYBPC3mut, TNNI3mut, HCMsmn, and LVHao was normalized to donor values after correction for myofibril density. However, Fmax was significantly lower in MYH7mut, TPM1mut, and TNNT2mut even after correction for myofibril density. In accordance, measurements in single myofibrils showed very low Fmax in MYH7mut, TPM1mut, and TNNT2mut compared with donor (respectively, 73 ± 3, 70 ± 7, 83 ± 6, and 113 ± 5 kN/m²). In addition, force was lower in MYH7mut cardiomyocytes compared with MYBPC3mut, HCMsmn, and donor at submaximal [Ca²⁺]. Low cardiomyocyte Fmax in HCM patients is largely explained by hypertrophy and reduced myofibril density. MYH7 mutations reduce force generating capacity of sarcomeres at maximal and submaximal [Ca²⁺]. These hypocontractile sarcomeres may represent the primary abnormality in patients with MYH7 mutations.

The coronary circulation and blood flow in left ventricular hypertrophy

Two distinct types of left ventricular hypertrophy (LVH) have been described: the so called "physiologic" hypertrophy, which is normally found in professional athletes, and "pathologic" LVH which is found in patients with inherited heart muscle disease such as hypertrophic cardiomyopathy (HCM) or patients with cardiac and systemic diseases characterized by pressure or volume overload. Patients with pathologic LVH have often symptoms and signs suggestive of myocardial ischemia despite normal coronary angiograms. Under these circumstances ischemia is due to coronary microvascular dysfunction (CMD). The abnormalities of the coronary microcirculation may be unrelated to the degree of LVH and cause a reduction in maximum myocardial blood flow which, in the absence of epicardial stenoses, is suggestive of CMD. There is no technique that enables direct visualization of coronary microcirculation in vivo in humans. Therefore, its assessment relies on the measurement of parameters which reflect its functional status, such as myocardial blood flow and coronary flow reserve which is an integrated measure of flow through both the large epicardial coronary arteries and the microcirculation. In this review article we discuss the pathophysiological mechanisms responsible for CMD in patients with primary and secondary LVH and how the recognition of this phenomenon is providing new important information on patient stratification and prognosis. Finally, we discuss how assessment of CMD may be used as a valuable surrogate marker to test the efficacy of old and new drugs. This article is part of a Special Issue entitled "Coronary Blood Flow".

Linksherzhypertrophie bei der Katze – «wenn eine hypertrophe Kardiomyopathie keine hypertrophe Kardiomyopathie ist»

According to WHO classification hypertrophic cardiomyopathy (HCM) is a primary genetic cardiomyopathy. Echocardiographically HCM is characterized by symmetric, asymmetric or focal left ventricular hypertrophy (LVH) without recognizable underlying physical cause. However, echocardiographically HCM in cats may not be distinguishable from other causes of a thick appearing left ventricle. Hypovolemia can look like a hypertrophied ventricle but is basically only pseudohypertrophic. Well recognized and logical physical causes of LVH include systemic hypertension and outflow obstruction. LVH similar to HCM may also be found in feline hyperthyroidism. The context of the disease helps to differentiate these physical / physiological causes of LVH. Difficult to distinguish from HCM, particularly when based on a snapshot of a single echocardiographic exam, are myocarditis and <<steroid-induced HCM>>. Only the clinical and echocardiographic course allow a reasonably confident etiological diagnosis and the differentiation between HCM and secondary LVH.

Non Sustained Ventricular Tachycardia in Hypertrophic Cardiomyopathy and New Ultrasonic Derived Parameters

The mechanism of sudden death in hypertrophic cardiomyopathy (HCM) is ventricular tachyarrhythmia emanating from myocyte disarray, fibrosis, and inhomogeneity in intramyocardial activation. Tissue synchronization imaging (TSI) allows the measurement of regional delay, while two-dimensional strain can be used to identify myocardial fibrosis. The aim of this study was to assess the relationship between new ultrasonically derived parameters and nonsustained ventricular tachycardia (NSVT) in patients with HCM. Ninety-three patients with HCM (mean age, 36 +/- 16 years) and 30 patients with hypertension with secondary left ventricular (LV) hypertrophy (mean age, 42 +/- 10 years; 65% men) were studied. All underwent standard echocardiographic, TSI, and two-dimensional strain examinations. Patients were followed every 3 months for 2 years. Holter monitoring was performed every 3 months. The primary endpoint was the occurrence of NSVT. Twenty-four patients (26%) had >or=1 episode of NSVT. Patients with NSVT had a higher value of maximal LV thickness (22 +/- 6 vs 19 +/- 5 mm, P = .04). There were no significant associations between NSVT on Holter monitoring and LV outflow gradient, New York Heart Association class, syncope, and medical therapy. N-terminal pro-brain natriuretic peptide values were significantly (P = .01) higher in patients with NSTV (1034 +/- 1088 vs 561 +/- 593 pg/mL). Patients with HCM and NSVT had (1) similar values on TSI-studied parameters to patients without NSVT, (2) significant reductions in basal and mid septal strain and in basal anterior-septal strain, and (3) more frequently peak systolic strain >or= -10% (P < .0001). In multivariate analysis, the presence of >3 LV segments with longitudinal two-dimensional strain >or= -10% (sensitivity, 81%; specificity, 97.1%; area under the curve, 0.944; P < .0001) was an independent predictor of NSVT. Using a simple, inexpensive, easily available, and bedside-usable tool, it was possible to recognize with good sensitivity and specificity patients with HCM at higher risk for NSVT.

Differentiation of Hypertrophic Cardiomyopathy and Cardiac Amyloidosis from Other Causes of Ventricular Wall Thickening by Two-Dimensional Strain Imaging Echocardiography

Hypertension is the most common cause of left ventricular (LV) hypertrophy. However, multiple causes can lead to LV hypertrophy, each of which has different histological and mechanical properties. To assess the value of a novel speckle-tracking echocardiographic measurement of myocardial strain and strain rate in defining the mechanical properties of LV hypertrophy, 20 patients with asymmetric hypertrophic cardiomyopathy, 24 patients with secondary LV hypertrophy, 12 patients with biopsy-proved confirmed cardiac amyloidosis, and 22 age-matched healthy asymptomatic volunteers were studied. Patients with amyloidosis had severe diastolic dysfunction, and myocardial deformation was significantly decreased. The new technique allowed cardiac amyloid to be easily differentiated from the other categories. In patients with hypertrophic cardiomyopathy, there was segmental myocardium dysfunction as assessed by strain imaging. LV global systolic velocity and radial displacement were higher, and abnormal relaxation was more frequent, in the group with secondary LV hypertrophy than in normal controls. In conclusion, the observations from strain parameters derived from speckle tracking were consistent with the known underlying pathology of each condition, which speaks to the value of strain imaging. Cardiac amyloid profoundly alters all strain parameters, and analysis of these parameters could aid in the diagnosis.

An Intraoperative Diagnosis of Dynamic Left Ventricular Outflow Tract Obstruction Using Transesophageal Echocardiography Leads to the Treatment with Intravenous Disopyramide

An Intraoperative Diagnosis of Dynamic Left Ventricular Outflow Tract Obstruction Using Transesophageal Echocardiography Leads to the Treatment with Intravenous Disopyramide

Comparison by real-time three-dimensional echocardiography of left ventricular geometry in hypertrophic cardiomyopathy versus secondary left ventricular hypertrophy

Calculation of left ventricular (LV) volume by 2-dimensional echocardiography (2DE) has been suboptimal due to the complex LV cavity geometry. Three-dimensional echocardiography (3DE) provides improved accuracy for LV volume and function compared with current 2D algorithms. 1 Siu S.C Levine R.A Rivera J.M Xie S.W Lethor J.P Three-dimensional echocardiography improves noninvasive assessment of left ventricular volume and performance. Am Heart J. 1995; 130: 812-822 Abstract Full Text PDF PubMed Scopus (67) Google Scholar Three-dimensional echocardiography is more accurate than standard 2D methods for measuring LV mass 2 Sapin P.M Gopal A.S Clarke G.B Smith M.D King D.L Three-dimensional echocardiography compared to two-dimensional echocardiography for measurement of left ventricular mass anatomic validation in an open chest canine model. Am J Hypertens. 1996; 9: 467-474 Crossref PubMed Scopus (28) Google Scholar and is a promising technique for calculation of LV ejection fraction, with excellent correlation with radionuclide angiography. 3 Nosir Y.F Fioretti P.M Vletter W.B Boersma E Salustri A Postma J.T Rejis A.E Ten Cate F.J Roelandt J.R Accurate measurement of left ventricular ejection fraction by three-dimensional echocardiography. A comparison with radionuclide angiography. Circulation. 1996; 94: 460-466 Crossref PubMed Scopus (158) Google Scholar We used real-time 3DE to evaluate total and segmental LV volume, ejection fraction, and myocardial mass in hypertrophic cardiomyopathy (HC) and compared the finding with those in patients with LV hypertrophy from other causes.

An Integrated Measure of Left Ventricular Diastolic Function Based on Relative Rates of Mitral E and A Wave Propagation

Background and objectives: The mitral E wave propagation inside the left ventricle is slowed in patients with abnormal left ventricular (LV) relaxation with a prolongation of its transit time to the LV outflow tract (T e). On the contrary, the mitral A wave propagation is faster in those with elevated LV end-diastolic stiffness, resulting in a shortening of its transit time (T a). We hypothesized that the T e/T a ratio may serve an integrated measure of global LV diastolic function. Methods and results: The T e/T a ratio was measured with Doppler echocardiography in 94 subjects: 25 normal subjects, 38 patients with LV hypertrophy (18 with secondary LV hypertrophy and 20 with hypertrophic cardiomyopathy), and 31 patients undergoing left heart catheterization for clinical indications. The T e/T a ratio was 1.98 ± 0.61 in the normal subjects, 3.32 ± 0.93 in patients with secondary LV hypertrophy ( P < .0001 vs normal), and 3.18 ± 1.36 in patients with hypertrophic cardiomyopathy ( P = .0003 vs normal). In the invasive group the T e/T a ratio (range 0.56 to 3.60) correlated significantly with Tau ( r = 0.76, P < .0001), peak negative dP/dt ( r = -0.46, P = .01), the LV late diastolic stiffness index ( r = 0.57, P = .0013), LV pre–A wave pressure ( r = 0.46, P = .0096), LV end-diastolic pressure ( r = 0.58, P = .0007), and the amount of LV pressure rise with atrial systole ( r = 0.52, P = .0032) but not with the heart rate. Tau and LV stiffness were its sole determinants by stepwise multiple regression (R = 0.82). Conclusions: The ratio of mitral E and A wave transit times inside the LV (T e/T a ratio) is closely related to LV relaxation, its late diastolic stiffness, and filling pressures and gives valuable insights into LV diastolic performance. (J Am Soc Echocardiogr 1999;12:811-6.)

Hypertensive Left Ventricular Hypertrophy with Left Ventricular Outflow Tract Obstructive Physiology: A Case of Successful Treatment with Dual-Chamber Pacing

Controversy exists over the use of atrioventricular synchronous pacing for patients with hypertrophic obstructive cardiomyopathy who are refractory to medical treatment. We present the case of an elderly man with severe-effort dyspnea attributable to hypertensive left ventricular hypertrophy with dynamic aortic outflow obstruction. We were able to achieve dramatic subjective and objective improvement in the exercise capacity of this patient with dual-chamber pacing after attempts at medical management had failed. This patient's response to therapy and his impressive response to minor pacemaker adjustments suggest that atrioventricular synchronous pacing should be considered for patients with secondary left ventricular hypertrophy as well as patients with hypertrophic obstructive cardiomyopathy.

Amplitudes, Durations, and Timings of Apically Directed Left Ventricular Myocardial Velocities: II. Systolic and Diastolic Asynchrony in Patients with Left Ventricular Hypertrophy

Background: Regional myocardial dysfunction may be the earliest manifestation of myocardial disease and can occur in the absence of abnormalities of global left ventricular (LV) function. The LV long-axis function, which is mainly due to subendocardial muscle fibers, may become abnormal in the presence of normal short-axis function. This study investigates the temporal and spatial characteristics of the LV long-axis function in patients with secondary LV hypertrophy in the presence of normal systolic function. Methods and Results: LV long-axis myocardial velocities were recorded in 18 patients with LV hypertrophy and preserved regional and global systolic function with Doppler tissue imaging. Apically directed myocardial velocities were recorded from the basal, mid, and apical segments of the four LV walls, and their amplitudes, timings, and durations were measured. The abnormalities uncovered by the analysis of regional myocardial velocities included (1) asynchrony in the onset of myocardial contraction circumferentially, (2) presence of postejection LV shortening, (3) asynchrony in the onset of early myocardial lengthening circumferentially, (4) reduced early myocardial lengthening velocity, (5) reduced early to late myocardial lengthening velocity and extents circumferentially, and (6) lack of variation in the basal myocardial velocities circumferentially in contrast to normal individuals. Conclusions:Patients with secondary LV hypertrophy with preserved regional and global systolic performance have distinct abnormalities in the timings and amplitudes of apically directed myocardial velocities. These abnormalities may explain some of the changes in LV global diastolic behavior and may also serve as markers of early regional myocardial dysfunction. (J Am Soc Echocardiogr 1998;11:112-8.)