Significant Diastolic Dysfunction Research Articles

Assessment of Right Ventricular and Right Atrial Systolic and Diastolic Performance Using Automated Border Detection.

Noninvasive assessment of right ventricular (RV) function is important clinically, but current techniques have limitations. Acoustic quantification (AQ) is an automated endocardial border detection technique that allows continuous determination of RV and right atrial (RA) area waveforms and may be useful for the assessment of RA and RV systolic and diastolic performance. Fifty patients (10 normal, 40 with RV pathology) were studied. Signal-averaged RA and RV AQ area waveforms were obtained and analyzed to compute parameters of diastolic and systolic function. All groups demonstrated significant diastolic dysfunction on the RA AQ waveform as manifested by a reduced percentage of passive atrial emptying and increased dependence on active atrial emptying. Abnormalities of diastolic performance were noted in all subgroups on RV AQ analysis as evidenced by a reduction in the percentage of ventricular filling occurring during early diastole and an increased contribution from active atrial contraction. This study demonstrates the feasibility of using automated analysis of signal-averaged RA and RV area waveforms for the evaluation of RV systolic and diastolic performance. This technique identified significant systolic and diastolic dysfunction in four groups of commonly seen right heart pathologies including biventricular heart failure, pulmonary hypertension, pressure and volume overloaded RVs, and biventricular hypertrophy.

No evidence for systolic or diastolic left ventricular dysfunction at rest in selected patients with long‐term Type I diabetes mellitus

We assessed left ventricular systolic and diastolic function using pulsed-waved Doppler echocardiography in a selected group of 20 patients with insulin-dependent diabetes mellitus (IDDM) (mean age, 35 +/- 8 years; mean diabetes duration, 17 + 7 years). Our patients were free of autonomic neuropathy and major micro- or macrovascular complications and had no evidence of ischemic heart disease or hypertension. The results were compared with those of 20 age- and sex-matched control subjects. We found that left ventricular geometry and mass, systolic function by M-mode and 2D-echocardiography, isovolumetric relaxation time, deceleration time and the PEP/LVET ratio were not significantly different between patients and control subjects. Hemodynamic parameters were also not significantly different except for a slightly higher heart rate in the patient group (75 +/- 11 vs. 68 + 6 bpm, P = 0.019). After correction of A-peak velocities for differences in heart rate, there was no significant difference of Doppler indices of diastolic left ventricular function between patients and control subjects. The absence of significant left ventricular systolic and diastolic dysfunction by Doppler echocardiography in our study patients may be explained by our patient selection. Left ventricular dysfunction in diabetic patients without concomitant hypertensive or ischemic heart disease may only occur in conjunction with microvascular disease in other organ systems, with autonomic neuropathy or with poor metabolic control.

Echocardiography in systemic lupus erythematosus.

Two dimensional echocardiography with doppler examination was performed in 54 patients with systemic lupus erythematosus (SLE). Nine (17%) had significant cardiac involvement (four left ventricular hypertrophy, one moderate pericardial effusion, one severe aortic regurgitation, and three ventricular systolic dysfunction). We further studied diastolic function in 45 patients who did not have a major abnormality in echo. SLE was graded as active in 16 patients (SLEDAI > 5) and inactive in 29 patients. Twenty age- and sex-matched subjects acted as controls. The data were compared using one way ANOVA test. Patients with active disease had significant diastolic dysfunction compared to inactive patients and controls as indicated by increased peak A (P < 0.01) and decreased E/A ratio (P < 0.01). There was no linear correlation between disease activity and diastolic dysfunction if SLEDAI was considered as a continuous variable (r=0.29 for E/A). Anticardiolipin antibodies (both IgG and IgM) were elevated in five patients (13 studied). One of them had severe mitral regurgitation, one had trace mitral and aortic regurgitation and one had diastolic dysfunction. We conclude that asymptomatic diastolic dysfunction is present in SLE patients.

A truncated cardiac troponin T molecule in transgenic mice suggests multiple cellular mechanisms for familial hypertrophic cardiomyopathy.

Mutations in multiple cardiac sarcomeric proteins including myosin heavy chain (MyHC) and cardiac troponin T (cTnT) cause a dominant genetic heart disease, familial hypertrophic cardiomyopathy (FHC). Patients with mutations in these two genes have quite distinct clinical characteristics. Those with MyHC mutations demonstrate more significant and uniform cardiac hypertrophy and a variable frequency of sudden death. Patients with cTnT mutations generally exhibit mild or no hypertrophy, but a high frequency of sudden death at an early age. To understand the basis for these distinctions and to study the pathogenesis of the disease, we have created transgenic mice expressing a truncated mouse cTnT allele analogous to one found in FHC patients. Mice expressing truncated cTnT at low (< 5%) levels develop cardiomyopathy and their hearts are significantly smaller (18-27%) than wild type. These animals also exhibit significant diastolic dysfunction and milder systolic dysfunction. Animals that express higher levels of transgene protein die within 24 h of birth. Transgenic mouse hearts demonstrate myocellular disarray and have a reduced number of cardiac myocytes that are smaller in size. These studies suggest that multiple cellular mechanisms result in the human disease, which is generally characterized by mild hypertrophy, but, also, frequent sudden death.

Hypertension and renal failure.

A 74-year-old man with a history of intermittent claudication, cigarette-smoking, hypertension, and a successful recent right nephro-ureterectomy for a right ureter transitional cell carcinoma, presented with abnormal renal function and...

Treatment of hypertrophic cardiomyopathy with coenzyme Q 10

Hypertrophic cardiomyopathy (HCM) is manifested by severe thickening of the left ventricle with significant diastolic dysfunction. Previous observations on the improvement in diastolic function and left ventricular wall thickness through the therapeutic administration of coenzyme Q 10 (CoQ 10) in patients with hypertensive heart disease prompted the investigation of its utility in HCM. Seven patients with HCM, six non-obstructive and one obstructive, were treated with an average of 200 mg/day of CoQ 10 with mean treatment whole blood CoQ 10 level of 2.9 μg/ml. Echocardiograms were obtained in all seven patients at baseline and again 3 or more months post-treatment. All patients noted improvement in symptoms of fatigue and dyspnea with no side effects noted. The mean interventricular septal thickness improved significantly from 1.51±0.17 cm to 1.14±0.13 cm, a 24% reduction ( P < 0.002). The mean posterior wall thickness improved significantly from 1.37±0.13 cm to 1.01±0.15 cm, a 26% reduction ( P<0.005). Mitral valve inflow slope by pulsed wave Doppler (EF slope) showed a non-significant trend towards improvement, 1.55±0.49 m/sec 2 to 2.58±1.18 m/sec 2 ( P<0.08). The one patient with subaortic obstruction showed an improvement in resting pressure gradient after CoQ 10 treatment (70 mmHg to 30 mmHg).

Iodine-123 Metaiodobenzylguanidine Scintigraphic Assessment of Myocardial Sympathetic Innervation in Patients With Familial Amyloid Polyneuropathy

Objectives. This study attempted to assess myocardial sympathetic innervation using iodine-123 (I-123) metaiodobenzylguanidine (MIBG) imaging in patients with familial amyloid polyneuropathy.Background. Signs and symptoms of cardiac autonomic dysfunction are commonly seen in patients with cardiac amyloidosis. However, the incidence and magnitude of abnormalities in myocardial sympathetic nerve function by means of I-123 MIBG imaging and their relation to clinical findings, cardiac function and the results of thallium-201 (Tl-201) and technetium-99m pyrophosphate (Tc-99m PYP) myocardial scanning have not yet been clarified.Methods. We performed M-mode, two-dimensional and Doppler echocardiography and I-123 MIBG, Tl-201 and Tc-99m PYP imaging of the heart in 12 patients with familial amyloid polyneuropathy and biopsy-proved cardiac amyloidosis.Results. Ten of 12 patients had no clinical evidence of overt heart disease, but left ventricular (LV) wall thickening was observed in 4 of these 10. Left ventricular percent fractional shortening and Doppler transmitral flow velocity patterns were found to be normal in all 12 patients. Eight of 12 patients showed no myocardial MIBG accumulation, with limited uptake in the remaining 4 demonstrated only in the LV anterior wall. Diffuse but mild myocardial uptake of Tc-99m PYP occurred in only 4 of 12 patients, and all 12 had normal results on Tl-201 myocardial scanning. Complete defects on myocardial MIBG scans were found in five of eight patients with negative findings on Tc-99m PYP myocardial scanning. The incidence and magnitude of myocardial uptake of MIBG were independent of clinical findings, extent of endomyocardial amyloid deposition, electrocardiographic QRS voltage and ventricular wall thickness.Conclusions. Patients with familial amyloid polyneuropathy show a high incidence of myocardial adrenergic denervation with viable myocardium that can be identified very early in cardiac amyloidosis, before the development of clinically apparent heart disease, ventricular wall thickening, significant LV systolic and diastolic dysfunction and positive findings on Tc-99m PYP myocardial scanning.(J Am Coll Cardiol 1997;29:168–74)>

Left ventricular diastolic function in hypertensive patients with unstable angina and single coronary artery disease

The present study was performed to investigate left ventricular diastolic (LVD) function in hypertensive patients with unstable angina. Three groups of 17 patients each were studied. Group 1 consisted of hypertensives with unstable angina (HTU); group 2, normotensives with unstable angina (NTU); and group 3, untreated, uncomplicated hypertensives (HT). The LVD function was assessed echocardiographically by transmitral valve Doppler flow to measure the ratio between the early diastolic filling (E) and the atrial contraction phase (A). An E/A ratio of < 1 was suggestive of LVD dysfunction. Left ventricular mass (LVM), from an M-mode echocardiogram using the Penn-Cube formula, was corrected to body surface area (LVM/S) using a standard nomogram. Data are represented as median values and analyzed by Mann-Whitney test. P was significant at < .05. The HTU group had an E/A ratio of 0.8, and the NTU and HT groups had ratios of 1.17 and 1.1, respectively. There was significant diastolic dysfunction in the HTU group compared with the NTU and HT groups (P = .037 and .049, respectively). Although the LVM/S was significantly higher in the HTU group when compared with the HT group (110.6 and 96.9, respectively, P = .017), there was no significant difference between the HTU and NTU groups (123.1), P = .67. Hypertensive patients with unstable angina have significant LVD dysfunction that seems to be independent of LVM and ischemia. This may be attributable to increased stiffness of the left ventricle or structural left ventricular abnormalities.

World atlas of holocene sea-level changes

In mice with temporally-induced cardiac-specific deficiency of acyl-CoA synthetase-1 (Acsl1H −/−), the heart is unable to oxidize long-chain fatty acids and relies primarily on glucose for energy. These metabolic changes result in the development of both a spontaneous cardiac hypertrophy and increased phosphorylated S6 kinase (S6K), a substrate of the mechanistic target of rapamycin, mTOR. Doppler echocardiography revealed evidence of significant diastolic dysfunction, indicated by a reduced E/A ratio and increased mean performance index, although the deceleration time and the expression of sarco/endoplasmic reticulum calcium ATPase and phospholamban showed no difference between genotypes. To determine the role of mTOR in the development of cardiac hypertrophy, we treated Acsl1H −/− mice with rapamycin. Six to eight week old Acsl1H −/− mice and their littermate controls were given i.p. tamoxifen to eliminate cardiac Acsl1, then concomitantly treated for 10 weeks with i.p. rapamycin or vehicle alone. Rapamycin completely blocked the enhanced ventricular S6K phosphorylation and cardiac hypertrophy and attenuated the expression of hypertrophy-associated fetal genes, including α-skeletal actin and B-type natriuretic peptide. mTOR activation of the related Acsl3 gene, usually associated with pathologic hypertrophy, was also attenuated in the Acsl1H −/− hearts, indicating that alternative pathways of fatty acid activation did not compensate for the loss of Acsl1. Compared to controls, Acsl1H −/− hearts exhibited an 8-fold higher uptake of 2-deoxy[1-14C]glucose and a 35% lower uptake of the fatty acid analog 2-bromo[1-14C]palmitate. These data indicate that Acsl1-deficiency causes diastolic dysfunction and that mTOR activation is linked to the development of cardiac hypertrophy in Acsl1H −/− mice.

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filing rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 ± 8 vs 81 ± 4 ml/m 2, p < 0.01) and end-systolic volume index (64 ± 7 vs 37 ± 4 ml/m 2, p < 0.001), but similar stroke volume index (41 ± 3 vs 43 ± 2 ml/m 2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and endsystolic volume indexes increased further (p < 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.