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PubMed2004

Pseudoexfoliation syndrome and asymptomatic myocardial dysfunction.

BACKGROUND: The purpose of this study was to investigate the frequency of asymptomatic left ventricular dysfunction in patients with pseudoexfoliation syndrome. METHODS: Two-dimensional and pulsed Doppler echocardiography of transmitral flow was performed on 27 patients with pseudoexfoliation syndrome, aged 66.9+/-5.6 years, and 24 healthy volunteers aged 63.9+/-6.5 years. Left ventricular (LV) systolic contraction and ejection were assessed by LV ejection fraction (EF) and fractional shortening (FS). LV diastolic filling parameters tested were: early fast diastolic filling (E wave), late diastolic filling (A wave), ratio E/A, velocity time integral E wave (VTIE) and A wave (VTIA), their ratio (VTIE/VTIA), pressure at the end of filling (LVEDP) and a pulmonary capillary wedge pressure (PCWP). RESULTS: Systolic parameters EF and FS, diastolic filling parameters such as A, LVEDP and PCWP were not significantly different between patients with pseudoexfoliation syndrome and controls (P>0.05). A significant difference (P<0.05) was found with regard to the diastolic filling parameters: E (61.6+/-15.1 vs 83.7+/-21.4), ratio E/A (0.8+/-0.1 vs 1.1+/-0.2), VTIE (8.6+/-1.8 vs 9.8+/-1.9), VTIA (10.3+/-2.4 vs 7.8+/-1.6) and ratio VTIA/VTIE (1.2+/-0.2 vs 0.8+/-0.2). CONCLUSION: Our study suggests the possibility of an association between patients with pseudoexfoliation syndrome and a discrete asymptomatic myocardial diastolic dysfunction.

Aged↗
PubMedDate not supplied

Clinical evaluation of left ventricular diastolic performance.

Diastole can be divided into four phases: isovolumic relaxation, early filling, diastasis, and atrial systole. The amount of LV filling that occurs during each of these phases depends on myocardial relaxation, the passive characteristics of the LV, the characteristics of the left atrium, pulmonary veins, and mitral valve, and the heart rate. When diastolic function is normal, the net effect of these factors results in an LV filling sufficient to produce an adequate cardiac output, while mean pulmonary venous pressure is maintained below 12 mm Hg. In the absence of systolic dysfunction, abnormal diastolic performance is usually due to abnormal relaxation and/or changes in the passive LV characteristics. Invasive studies can quantitate the rate of myocardial relaxation and the LV diastolic pressure-volume relation. More recently, RNA and Doppler echocardiography have been used to noninvasively evaluate diastolic performance by determining the pattern of LV diastolic filling. At rest, most LV filling occurs early in diastole. Conditions that produce diastolic dysfunction, such as LV hypertrophy and ischemia, are associated with reduced early diastolic filling and an augmented importance of atrial systole. It is important to recognize that such patterns can occur in patients who do not have clinically apparent diastolic dysfunction and in normals. Furthermore, a normal pattern can occur in patients who have severe diastolic dysfunction. A reduced early diastolic filling, in the absence of pulmonary congestion, indicates the loss of diastolic reserve, since the left atrium is being used as a booster pump. This pattern of diastolic filling in a patient who has symptoms of pulmonary congestion may suggest diastolic dysfunction, even if the systolic LV performance is normal. Since diastolic filling of the LV results from a complex interplay of factors, it is unlikely that a single, easily interpreted index of LV diastolic performance will ever be developed. However, the recent development of a noninvasive evaluation of the pattern of LV diastolic filling by RNA or Doppler echocardiography is an important advance. When interpreted with an understanding of the determinants of LV filling and the patient's clinical status, these noninvasive tests can contribute to the rational assessment of LV diastolic performance.

Animals↗
PubMed1993

Cardiovascular aspects in renal disease.

The majority of hemodialysis patients die from cardiovascular disease. However, the contribution of myocardial infarction to mortality is relatively minor, despite the fact that coronary artery disease is common in uremic patients. Hypertension seems to be the major risk factor for the development of atherosclerosis in hemodialysis patients, although abnormalities of the lipid spectrum, characterized by an increase in triglycerides and very low density lipoprotein levels and a decrease in high-density lipoprotein levels, are frequent in hemodialysis patients. The existence of left ventricular (LV) hypertrophy is a serious risk factor for morbidity and mortality in hemodialysis patients. LV hypertrophy can present as a dilated cardiomyopathy or as concentric or asymmetric septal hypertrophy. Loss of myocardial contractility by coronary artery disease or carnitine deficiency can lead to systolic LV dysfunction with a compensatory dilated cardiomyopathy. Furthermore, the presence of a hypercirculation in uremic patients, resulting from anemia, the arteriovenous fistula, or fluid overload, can also lead to a dilated cardiomyopathy. Systolic LV dysfunction occurs when the increase in LV wall thickness is inadequate for the increase in LV radius, which might be caused by increased levels of parathyroid hormone. LV diastolic dysfunction, resulting from an increase in LV mass due to the effects of hypertension or to uremic interstitial fibrosis, can both lead to pulmonary edema and hypotensive periods during hemodialysis and is a severe risk factor for mortality in hemodialysis patients. Therefore, in uremic patients, anemia should be corrected and hypertension adequately treated early in the development of renal failure. Chronic fluid overload should be prevented by adequate estimation of optimal dry weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗
PubMed2006

Inhibition of NF-{kappa}B improves left ventricular remodeling and cardiac dysfunction after myocardial infarction.

Several studies have demonstrated that NF-kappaB is substantially involved in the progression of cardiac remodeling; however, it remains uncertain whether the continuous inhibition of NF-kappaB is effective for the prevention of myocardial remodeling. Myocardial infarction (MI) was produced by ligation of the left anterior coronary artery of rats. IMD-0354 (10 mg/kg per day), a novel phosphorylation inhibitor of IkappaB that acts via inhibition of IKK-beta, was injected intraperitoneally starting 24 h after induction of MI for 28 days. After 28 days, the IMD-0354-treated group showed significantly improved survival rate compared with that of the vehicle-treated group (P < 0.05). Although infarct size was similar in both groups, improved left ventricular (LV) remodeling and diastolic dysfunction, as indicated by smaller LV cavity (LV end-diastolic area: vehicle, 74.13 +/- 3.57 mm(2); IMD-0354, 55.00 +/- 3.73 mm(2); P < 0.05), smaller peak velocity of early-to-late filling wave (E/A) ratio (vehicle, 3.87 +/- 0.26; IMD-0354, 2.61 +/- 0.24; P < 0.05), and lower plasma brain natriuretic peptide level (vehicle, 167.63 +/- 14.87 pg/ml; IMD-0354, 110.75 +/- 6.41 pg/ml; P < 0.05), were observed in the IMD-0354-treated group. Moreover, fibrosis, accumulation of macrophages, and expression of several factors (transforming growth factor-beta1, monocyte chemoattractant protein-1, matrix metalloproteinase-9 and -2) in the noninfarcted myocardium was remarkably inhibited by IMD-0354. In conclusion, inhibition of NF-kappaB activation may reduce the proinflammatory reactions and modulate the extracellular matrix and provide an effective approach to prevent adverse cardiac remodeling after MI.

Animals↗
PubMed1985

Intact systolic left ventricular function in clinical congestive heart failure.

Clinical congestive heart failure (CHF) is traditionally associated wtih significant left ventricular (LV) systolic dysfunction. Over a 1-year period, 58 patients with CHF and intact systolic function (LV ejection fraction [EF] 62 +/- 11%) were identified. An objective clinical-radiographic CHF score was used to document the clinical impression. Based on radionuclide evaluation of peak filling rate, 38% of these patients were found to have a significant abnormality in diastolic function as measured by peak filling rate (less than 2.50 end-diastolic volume/s). An additional 24% of the patients had probable diastolic dysfunction with borderline abnormal peak filling rate measurements (2.5 to 3.0 end-diastolic volume/s). The disease states most frequently associated with CHF and intact systolic function were coronary artery disease and systemic hypertension. During a 3-month sampling period 42% of patients with clinical diagnosis of CHF referred to the nuclear cardiology laboratory were found to have intact systolic function; thus, intact systolic function is not uncommon in patients with clinical CHF. Abnormal diastolic function is the most frequently encountered mechanism for the occurrence of CHF. Definition of systolic and diastolic function appears relevant for development of optimal therapeutic strategies for the treatment of patients with CHF.

Adult↗
PubMed2006

Relation of B-type natriuretic peptide early after acute myocardial infarction to left ventricular diastolic function and extent of myocardial damage determined by magnetic resonance imaging.

Early after acute myocardial infarction, the relation between plasma B-type natriuretic peptide (BNP) and extent of myocardial scar formation and diastolic dysfunction remains unclear. In 32 consecutive patients early (5 +/- 3 days) after a first acute myocardial infarction, delayed contrast-enhanced magnetic resonance (MR) imaging was performed to define myocardial scar. Diastolic function was assessed using phase-contrast MR measurements of mitral flow and septal tissue velocities (tissue MR imaging) to estimate left ventricular (LV) filling pressures. MR study was immediately followed by BNP measurement. BNP related to LV ejection fraction (r = -0.52, p = 0.002), extent of myocardial scar (percent delayed hyperenhancement of LV mass, r = 0.49, p = 0.005; transmural index, r = 0.58, p <0.001), and estimated LV filling pressures (ratio of early diastolic mitral flow velocity to early diastolic mitral annular velocity, r = 0.51, p = 0.003). In multivariate analysis, transmural index and early diastolic mitral flow velocity/early diastolic mitral annular velocity were independent predictors of BNP levels (p <0.05, power of 0.99 at alpha = 0.05). In conclusion, among patients with recent myocardial infarction, high BNP levels are independently associated with extent of myocardial scar tissue and estimated LV filling pressures.

Blood Flow Velocity↗
PubMedDate not supplied

Doppler echocardiographic index for assessment of global right ventricular function.

Echocardiographic assessment of right ventricular function remains difficult and challenging. However, there is considerable clinical need for a simple, reproducible, and reliable parameter of right ventricular function in patients with right-sided heart disease. The purpose of this study was to assess the clinical value of a Doppler-derived index, combining systolic and diastolic intervals of the right cycle, in assessing global right ventricular function in patients with primary pulmonary hypertension. The study population comprised 26 consecutive patients with primary pulmonary hypertension and 37 age-matched normal subjects. The sum of right ventricular isovolumetric contraction time and isovolumetric relaxation time was obtained by subtracting right ventricular ejection time from the interval between cessation and onset of the tricuspid inflow velocities with pulsed-wave Doppler echocardiography. An index of combined right ventricular systolic and diastolic function was obtained by dividing the sum of both isovolumetric intervals by ejection time. The index was compared with available parameters of systolic or diastolic function, clinical symptoms, and survival. Right ventricular isovolumetric contraction time and isovolumetric relaxation time were prolonged significantly in patients with primary pulmonary hypertension (85 +/- 41 msec and 135 +/- 43 msec) compared with normal subjects (38 +/- 7 msec and 49 +/- 9 msec, respectively; p < 0.001). Ejection time was shortened significantly in patients with pulmonary hypertension (241 +/- 43 msec versus normal [322 +/- 21 msec]; p < 0.001). However, the index was the single most powerful variable to discriminate patients with primary pulmonary hypertension from normal subjects (0.93 +/- 0.34 versus 0.28 +/- 0.04; p < 0.001) and was the strongest predictor of clinical status and survival. The index was not significantly affected by heart rate, right ventricular pressure, right ventricular dilation, or tricuspid regurgitation. It is well known that right ventricular systolic and diastolic dysfunction coexist in patients with primary pulmonary hypertension. This article reports the use of an easily obtainable Doppler-derived index that combines elements of systolic and diastolic function. This index appears to be a useful noninvasive means that correlates with symptoms and survival in patients with primary pulmonary hypertension.

Adult↗
PubMed1994

Cardiac involvement in Ribbing's disease.

Cardiac involvement was assessed in 14 patients with Ribbing's disease, a rare hereditary sclerosing bone dysplasia. When compared to age-, sex- and blood pressure-matched controls, the patients with Ribbing's disease had significant alterations in left ventricular systolic and diastolic function and an impaired exercise tolerance. Supraventricular and ventricular arrhythmias also tended to be more frequent in these patients than in controls. In conclusion, Ribbing's disease, initially described as a skeletal disease only, also involves the cardiovascular system. Despite its rarity, the expression of the disease is easily followed and identification of the genetic defect could shed some new light on the pathophysiological mechanisms linking hypertension, myocardial hypertrophy and diastolic dysfunction.

Adolescent↗
PubMed2001

Load as an acute determinant of end-diastolic pressure-volume relation.

Afterload-induced changes in myocardial relaxation are a mechanism for diastolic dysfunction when afterload is elevated beyond certain limits. The present study investigated the effects of acute afterload and preload changes on the position of the end-diastolic (ED) pressure-volume (P-V) relation. Beat-to-beat afterload elevations were induced in seven open-chest rabbits by gradually occluding the ascending aorta to increase peak left ventricular pressure (LVP) from baseline to isovolumetric level. Afterload elevations were performed at three ED LVP: 2.0 +/- 0.2 (low), 5.7 +/- 0.2 (mid), and 9.6 +/- 0.6 (high) mmHg. Preload was altered with caval occlusions and/or intravenous dextran. Afterload elevations induced an upward shift of the diastolic P-V relation, which became more important as afterload and/or preload increased. For instance, maximal afterload elevations shifted this relation upward 2.2 +/- 0. 5, 5.1 +/- 0.8, and 12.1 +/- 1.7 mmHg at low, mid, and high preload, respectively. These effects were partially due to changes in relaxation rate and time available to relax. In conclusion, load is an acute determinant of the ED P-V relation, which, therefore, does not provide a load-independent assessment of diastolic function.

Animals↗
PubMed1995

Congestive heart failure in patients with valvular aortic stenosis. A clinical and echocardiographic Doppler study.

The aim of this study was to evaluate echographically anatomic and functional features of the left ventricle in adult patients with valvular aortic stenosis according to the presence or absence of congestive heart failure and the level of ventricular performance. Fifty-six adult patients with moderate-to-severe aortic stenosis underwent echocardiographic Doppler examination in order to evaluate left ventricular mass and dimensions, systolic function and filling dynamics. Twenty-seven patients had no heart failure and were symptomatic for angina (5), syncope (4) or were symptom-free (group I); the other 29 had heart failure (group II): 16 with normal left ventricular systolic performance (fractional shortening > 25%, group IIa) and 13 with systolic dysfunction (fractional shortening < or = 25%, group IIb). Despite a similar left ventricular mass, compared to group IIa, group IIb showed a significant left ventricular dilatation (end-diastolic diameter: 61 +/- 6.5 vs. 45.5 +/- 6.1 mm, p < 0.001) and mild or no increase in wall thickness (11.5 +/- 1.6 vs. 14.9 +/- 2 mm, p < 0.001). Indices of left ventricular filling on Doppler transmitral flow were also significantly different between the two groups, with a higher early-to-late filling ratio and a shorter deceleration time of early filling in group IIb (2.8 +/- 1.9 vs. 1.2 +/- 0.85, p < 0.01, and 122 +/- 66 vs. 190 +/- 87 ms, p < 0.05, respectively), both indirectly indicating higher left atrial pressure. Finally, heart failure was generally more severe in group IIb patients. In some patients with aortic stenosis, symptoms of heart failure may be present despite a normal left ventricular systolic function and seem to depend on abnormalities of diastolic function. The presence of systolic or isolated diastolic dysfunction appears to be related to a different geometric adaptation of the left ventricle to chronic pressure overload.

Aged↗
PubMed1993

Intraventricular early diastolic filling during acute myocardial ischemia, assessment by multigated color m-mode Doppler echocardiography.

BACKGROUND: Color M-mode Doppler echocardiography has been suggested as a new noninvasive technique for assessing left ventricular diastolic function. The present study investigated intraventricular filling pattern by color M-mode Doppler in patients during percutaneous transluminal coronary angioplasty (PTCA). In a dog model of myocardial ischemia, the color M-mode flow pattern was related to indices of global and regional myocardial function. METHODS AND RESULTS: From color M-mode images, the time difference (TD) between occurrence of peak velocity in the apical region and at the mitral tip was determined in 20 patients and eight anesthetized dogs during coronary occlusions. During PTCA, the timing of peak velocity was progressively delayed from mitral valve to apex. Consistent with this, the dog model showed delayed apical filling during coronary occlusion; TD increased from 18 +/- 4 to 71 +/- 9 milliseconds (P < .01). In the ischemic region, systolic shortening (sonomicrometry) decreased from 20 +/- 3% to -5 +/- 2% (p < .01). The one-third filling fraction decreased from 59 +/- 5% to 31 +/- 6% (P < .01) and correlated with TD (r = .85, P < .01). The time constant of isovolumic relaxation (tau) increased slightly and correlated with TD (r = .81, P < .01). Pacing tachycardia, caval constriction, and volume loading were performed to mimic the ischemia-induced changes in heart rate, stroke volume, and intracavitary filling pressure, respectively. There were no significant changes in TD or tau during these interventions. CONCLUSIONS: Color M-mode Doppler echocardiography showed a marked delay of apical peak filling velocity during PTCA. The experimental data suggest that this reflects retarded filling of the ischemic ventricle. Thus, color M-mode Doppler may provide a useful method for assessing diastolic dysfunction.

Adult↗
PubMed1985

Right ventricular systolic and diastolic function at rest in patients with coronary artery disease. Assessment with equilibrium radionuclide ventriculography.

Right ventricular systolic and diastolic function was studied in patients with ischemic heart disease using equilibrium radionuclide ventriculography. In patients with inferior myocardial infarction and proximal right coronary lesions, the right ventricular ejection fraction (0.43 +/- 0.06, n = 10, mean +/- SD) and peak filling rate (1.7 +/- 0.4 EDV/sec) were lower than normals (0.57 +/- 0.07 and 2.7 +/- 0.4 EDV/sec, n = 10, p less than 0.001, respectively). In these patients, the right ventricular time to peak filling rate was longer than in normals (225 +/- 36 msec vs 136 +/- 45 msec, p less than 0.001), while the left ventricular ejection fraction remained normal. In patients with inferior myocardial infarction and distal right coronary lesions, the right ventricular ejection fraction, peak filling rate and time to peak filling rate were not different from those in normals. Even in patients with proximal right coronary lesions, the right ventricular ejection fraction was normal unless they had an inferior myocardial infarction. A decreased left ventricular ejection fraction and abnormal motion of the ventricular septum did not affect the right ventricular ejection fraction. The present results suggest that patients with an inferior myocardial infarction and proximal right coronary lesion often develop right ventricular systolic and diastolic dysfunction.

Adult↗
PubMed2004

Role of diastole in left ventricular function, I: Biochemical and biomechanical events.

Left ventricular diastolic function plays an important role in cardiac physiology. Lusitropy, the ability of the cardiac myocytes to relax, is affected by both biochemical events within the myocyte and biomechanical events in the left ventricle. Beta-adrenergic stimulation alters diastole by enhancing the phosphorylation of phospholamban, a substrate within the myocyte that increases the uptake of calcium ions into the sarcoplasmic reticulum, increasing the rate of relaxation. Troponin I, a regulatory protein involved in the coupling of excitation to contraction, is vital to maintaining the diastolic state; depletion of troponin I can produce diastolic dysfunction. Other biochemical events, such as defects in the voltage-sensitive release mechanism or in inositol triphosphate calcium release channels, have also been implicated in altering diastolic tone. Extracellular collagen determines myocardial stiffness; impaired glucose tolerance can induce an increase in collagen cross-linking and lead to higher end-diastolic pressures. The passive properties of the left ventricle are most accurately measured during the diastasis and atrial contraction phases of diastole. These phases of the cardiac cycle are the least affected by volume status, afterload, inherent viscoelasticity, and the inotropic state of the myocardium. Diastolic abnormalities can be conceptualized by using pressure-volume loops that illustrate myocardial work and both diastolic and systolic pressure-volume relationships. The pressure-volume model is an educational tool that can be used to demonstrate isolated changes in preload, afterload, inotropy, and lusitropy and their interaction.

Action Potentials↗
PubMed2006

Early diastolic mitral annular velocity and color M-mode flow propagation velocity in the evaluation of left ventricular diastolic function in patients with Fabry disease.

Fabry disease is an X-linked genetic disorder characterized by progressive intracellular accumulation of neutral glycosphingolipids. Cardiac involvement is frequent and left ventricular (LV) diastolic dysfunction is present in most of the affected subjects. Pulsed-wave tissue Doppler echocardiography (PW-TDE) and color M-mode are new Doppler methods for LV diastolic function evaluation. Their role in the assessment of Fabry disease-related cardiomyopathy remains to be established. In this study we aimed to determine the utility of PW-TDE and color M-mode-derived parameters in the assessment of LV diastolic function in patients with Fabry disease. Eighty-one echocardiographic examinations performed in 35 patients affected by Fabry disease were retrospectively analyzed. Early diastolic lateral mitral annular velocity (E(m)) determined by PW-TDE and color M-mode flow propagation velocity (V(p)) were measured and compared to LV filling patterns obtained using standard Doppler indexes. The receiver operating characteristics (ROC) curves method was used to determine the summary measure of relative accuracy for E(m) and V(p). A comparison of ROC curves showed a significant difference for areas under the curve in favor of E(m) (P < 0.001). Pseudonormal filling pattern, higher LV mass index, higher relative wall thickness, larger left atrial diameter, and older age were more frequent (all P < 0.001) in patients with incorrect diagnosis of normal LV diastolic function based on the measurement of V(p). E(m) appears to be superior to V(p) in the assessment of LV diastolic function in patients with Fabry disease. V(p) fails to detect abnormal LV diastolic function in subjects with pronounced concentric LV remodeling and pseudonormal filling pattern.

Adult↗
PubMedDate not supplied

Role of exercise and metabolism in heart failure with normal ejection fraction.

Left ventricular dysfunction associated with metabolic disorders has a number of features that might shed light on the integrity of heart failure with normal ejection fraction. First, although these patients may be dyspneic and have a normal ejection fraction, their diastolic dysfunction is not isolated. Both experimental models and sensitive new parameters in humans have shown abnormal systolic function, even though the less sensitive parameters (such as ejection fraction) become abnormal only with stress. Moreover, the mechanistic contributors to myocardial dysfunction, including structural changes and metabolic influences on the cardiac myocyte, interstitial fibrosis, vascular disease, and altered loading, are likely to influence systolic as much as diastolic function. The responses of systolic and diastolic heart failure to exercise training show analogies, particularly with respect to the importance of peripheral adaptation, as well as a similar training response. Together, these features are more supportive of a continuum of pathophysiology between systolic and diastolic heart failure, rather than the 2 representing discreet phenomena.

Animals↗
PubMed2005

Antihypertensive drugs and the heart.

The main goal of current antihypertensive therapy is to achieve a lowering of intra-arterial pressure by various mechanisms. A plethora of data suggests that this reduces cardiovascular morbidity and mortality due to stroke, heart failure and to a lesser extent, ischemic heart disease. Early cardiac manifestations of chronic hypertension, left ventricular hypertrophy (LVH) and diastolic dysfunction (CHF-D) confer additional risk of cardiovascular morbidity and mortality in patients with hypertension. Regression of left ventricular (LV) mass with antihypertensive therapy is associated with improved diastolic function and overall reduction in cardiovascular events, and this benefit may be independent of actual lowering of arterial pressure. Antihypertensive therapy should therefore be geared to both lower arterial blood pressure and specifically reverse pathophysiologic processes that promote LVH and CHF-D. Emerging therapies accomplish this without specifically affecting blood pressure. Therefore, future treatments for hypertension may require a combination of drugs performing complimentary tasks in lowering arterial pressure and reversing maladaptive physiologic and genetic processes causing hypertensive heart disease. This review summarizes the current and emerging approaches to the treatment of individuals with hypertensive heart disease.

Antihypertensive Agents↗
PubMedDate not supplied

Characterization and quantitation of extracellular collagen matrix in myocardium of pigs with spontaneously occurring hypertrophic cardiomyopathy.

The extracellular matrix between cardiocytes has been suggested to play an important role in maintaining the structure and function of the heart. The purpose of this study was to elucidate the morphological changes in the collagen of the extracellular matrix (ECM) in the hearts of pigs with hypertrophic cardiomyopathy. Sixty pigs diagnosed with hypertrophic cardiomyopathy from 605 purebred Landrace pigs ages 6 to 9 months were used in this study. Morphologically, these pigs with hypertrophic cardiomyopathy had increased heart weight and heart-to-body weight ratio, thickening of the left ventricular (LV) and right ventricular (RV) free walls and septum, disorientation of cardiocytes, myocardial fibrosis, and intramural coronary arteriosclerosis. Similar observations have been described in our preliminary report (Cardiovasc Pathol 3:261, 1994). In the present study, we have modified the silver impregnation technique to stain paraffin-embedded sections to demonstrate three types of ECM. There were endomysial struts, perimysial weaves, and epimysial coils in the myocardium. The light microscopic findings of the struts, weaves, and coils were also confirmed by scanning electromicroscopic examination. The numbers of these fine structures were increased significantly in the pigs with hypertrophic cardiomyopathy. In addition, the amounts of collagen in the LVs, RVs, and septum (Sep) in pigs with hypertrophic cardiomyopathy (LV = 19.37+/-0.79, RV = 23.72+/-0.72, Sep = 20.38+/-0.94 microg/mg, n = 60) were significantly higher (p < 0.01) than that in similar areas of normal pigs (LV = 14.56+/-1.11, RV = 18.90+/-1.02, Sep = 14.99+/-1.33 microg/mg, n = 30, respectively). Our findings of an overall increase of collagen content suggested that the accumulation of collagen matrix might be another factor responsible for the diastolic dysfunction of hypertrophic cardiomyopathy. These results might also infer that the increased collagen matrix could contribute to the stiffness of the cardiac chambers, thereby markedly affecting systolic and diastolic function of the heart. These observations provide further support that the pig may be an animal model for human cardiovascular disease.

Animals↗
PubMed1986

Angina pectoris early after myocardial infarction: clinical experience of the multicentre post-infarction program.

In the Multicenter Post Infarction Program, 33% of 867 patients had early angina pectoris, i.e. angina between 2 days and hospital discharge 17 +/- 9 days after infarction. Early post-infarction angina was not significantly associated with cardiac death during 2.5 years of follow-up whereas both ventricular arrhythmias and left ventricular dysfunction were strongly and independently related to subsequent mortality. After myocardial infarction, there is no significant association between early angina pectoris and either ventricular arrhythmias or systolic or diastolic dysfunction of the left ventricle. However, patients with early post-infarction angina were one-and-a-half times as likely to be rehospitalized and two-and-a-half times as likely to experience recurrent non-fatal myocardial infarction during the year after myocardial infarction. Exercise angina pectoris was associated with subsequent mortality but not with recurrent non-fatal myocardial infarction. ST segment depression greater than or equal to 1 mm or greater than or equal to 2 mm during exercise was not significantly associated with either subsequent death or non-fatal myocardial infarction.

Adrenergic beta-Antagonists↗