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Biomedical subjects

Thomas H Marwick

Publications and source records attributed to Thomas H Marwick.

At least 73 records · Page 4Linked to original sources
PubMed2004

Quantitative myocardial contrast echocardiography for prediction of thrombolysis in myocardial infarction flow in acute myocardial infarction.

Clinical evaluation of arterial patency in acute ST-elevation myocardial infarction (STEMI) is unreliable. We sought to identify infarction and predict infarct-related artery patency measured by the Thrombolysis In Myocardial Infarction (TIMI) score with qualitative and quantitative intravenous myocardial contrast echocardiography (MCE). Thirty-four patients with suspected STEMI underwent MCE before emergency angiography and planned angioplasty. MCE was performed with harmonic imaging and variable triggering intervals during intravenous administration of Optison. Myocardial perfusion was quantified offline, fitting an exponential function to contrast intensity at various pulsing intervals. Plateau myocardial contrast intensity (A), rate of rise (beta), and myocardial flow (Q = A x beta) were assessed in 6 segments. Qualitative assessment of perfusion defects was sensitive for the diagnosis of infarction (sensitivity 93%) and did not differ between anterior and inferior infarctions. However, qualitative assessment had only moderate specificity (50%), and perfusion defects were unrelated to TIMI flow. In patients with STEMI, quantitatively derived myocardial blood flow Q (A x beta) was significantly lower in territories subtended by an artery with impaired (TIMI 0 to 2) flow than those territories supplied by a reperfused artery with TIMI 3 flow (10.2 +/- 9.1 vs 44.3 +/- 50.4, p = 0.03). Quantitative flow was also lower in segments with impaired flow in the subtending artery compared with "normal" patients with TIMI 3 flow (42.8 +/- 36.6, p = 0.006) and all segments with TIMI 3 flow (35.3 +/- 32.9, p = 0.018). An receiver-operator characteristic curve derived cut-off Q value of <11.3, representing impaired myocardial flow, was 73% sensitive and 67% specific for TIMI <3 flow at angiography. Thus, qualitative MCE identifies patients with STEMI but provides no information regarding infarct-related artery patency, whereas quantitative MCE can predict impaired flow in patients with acute STEMI.

Coronary Angiography↗
PubMed2004

Exercise training for patients with heart failure: a systematic review of factors that improve mortality and morbidity.

PURPOSE: To determine the efficacy of exercise training and its effects on outcomes in patients with heart failure. METHODS: MEDLINE, Medscape, and the Cochrane Controlled Trials Registry were searched for trials of exercise training in heart failure patients. Data relating to training protocol, exercise capacity, and outcome measures were extracted and reviewed. RESULTS: A total of 81 studies were identified: 30 randomized controlled trials, five nonrandomized controlled trials, nine randomized crossover trials, and 37 longitudinal cohort studies. Exercise training was performed in 2387 patients. The average increment in peak oxygen consumption was 17% in 57 studies that measured oxygen consumption directly, 17% in 40 studies of aerobic training, 9% in three studies that only used strength training, 15% in 13 studies of combined aerobic and strength training, and 16% in the one study on inspiratory training. There were no reports of deaths that were directly related to exercise during more than 60,000 patient-hours of exercise training. During the training and follow-up periods of the randomized controlled trials, there were 56 combined (deaths or adverse events) events in the exercise groups and 75 combined events in the control groups (odds ratio [OR] = 0.98; 95% confidence interval [CI]: 0.61 to 1.32; P = 0.60). During this same period, 26 exercising and 41 nonexercising subjects died (OR = 0.71; 95% CI: 0.37 to 1.02; P = 0.06). CONCLUSION: Exercise training is safe and effective in patients with heart failure. The risk of adverse events may be reduced, but further studies are required to determine whether there is any mortality benefit.

Exercise↗
PubMed2004

Impact of scar thickness on the assessment of viability using dobutamine echocardiography and thallium single-photon emission computed tomography: a comparison with contrast-enhanced magnetic resonance imaging.

OBJECTIVES: We sought to determine whether the transmural extent of scar (TES) explains discordances between dobutamine echocardiography (DbE) and thallium single-photon emission computed tomography (Tl-SPECT) in the detection of viable myocardium (VM). BACKGROUND: Discrepancies between DbE and Tl-SPECT are often attributed to differences between contractile reserve and membrane integrity, but may also reflect a disproportionate influence of nontransmural scar on thickening at DbE. METHODS: Sixty patients (age 62 +/- 12 years; 10 women and 50 men) with postinfarction left ventricular dysfunction underwent standard rest-late redistribution Tl-SPECT and DbE. Viable myocardium was identified when dysfunctional segments showed Tl activity >60% on the late-redistribution image or by low-dose augmentation at DbE. Contrast-enhanced magnetic resonance imaging (ceMRI) was used to divide TES into five groups: 0%, <25%, 26% to 50%, 51% to 75%, and >75% of the wall thickness replaced by scar. RESULTS: As TES increased, both the mean Tl uptake and change in wall motion score decreased significantly (both p < 0.001). However, the presence of subendocardial scar was insufficient to prevent thickening; >50% of segments still showed contractile function with TES of 25% to 75%, although residual function was uncommon with TES >75%. The relationship of both tests to increasing TES was similar, but Tl-SPECT identified VM more frequently than DbE in all groups. Among segments without scar or with small amounts of scar (<25% TES), >50% were viable by SPECT. CONCLUSIONS: Both contractile reserve and perfusion are sensitive to the extent of scar. However, contractile reserve may be impaired in the face of no or minor scar, and thickening may still occur with extensive scar.

Adrenergic beta-Agonists↗
PubMed2004

Patients with a hypertensive response to exercise have impaired systolic function without diastolic dysfunction or left ventricular hypertrophy.

OBJECTIVES: We sought to determine if a hypertensive response to exercise (HRE) is associated with myocardial changes consistent with early hypertensive heart disease. BACKGROUND: An HRE predicts the development of chronic hypertension (HT) and may reflect a preclinical stage of HT. METHODS: Patients with a normal left ventricular (LV) ejection fraction and a negative stress test were recruited into three matched groups: 41 patients (age 56 +/- 10 years) with HRE (>210/105 mm Hg in men; >190/105 in women), comprising 22 patients with (HT+) and 19 without resting hypertension (HT-); and 17 matched control subjects without HRE. Long-axis function was determined by measurement of the strain rate (SR), peak systolic strain, and cyclic variation (CV) of integrated backscatter in three apical views. RESULTS: An HRE was not associated with significant differences in LV mass index. Exercise performance and diastolic function were reduced in HRE(HT+) patients, but similar in HRE(HT-) patients and controls. Systolic dysfunction (peak systolic strain, SR, and CV) was significantly reduced in HRE patients (p < 0.001 for all). These reductions were equally apparent in patients with and without a history of resting HT (p = NS) and were independent of LV mass index and blood pressure (p < 0.01). CONCLUSIONS: An HRE is associated with subtle systolic dysfunction, even in the absence of resting HT. These changes occur before the development of LV hypertrophy or detectable diastolic dysfunction and likely represent early hypertensive heart disease.

Exercise↗
PubMed2004

The relative importance of vascular structure and function in predicting cardiovascular events.

OBJECTIVES: We sought to assess the prognostic utility of brachial artery reactivity (BAR) in patients at risk of cardiovascular events. BACKGROUND: Impaired flow-mediated vasodilation measured by BAR is a marker of endothelial dysfunction. Brachial artery reactivity is influenced by risk factors and is responsive to various pharmacological and other treatments. However, its prognostic importance is uncertain, especially relative to other predictors of outcome. METHODS: A total of 444 patients were prospectively enrolled to undergo BAR and follow-up. These patients were at risk of cardiovascular events, based on the presence of risk factors or known or suspected cardiovascular disease. We took a full clinical history, performed BAR, and obtained carotid intima-media thickness (IMT) and left ventricular mass and ejection fraction. Patients were followed up for cardiovascular events and all-cause mortality. Multivariate Cox regression analysis was performed to assess the independent association of investigation variables on outcomes. RESULTS: The patients exhibited abnormal BAR (5.2 +/- 6.1% [mean +/- SD]) but showed normal nitrate-mediated dilation (9.9 +/- 7.2%) and normal mean IMT (0.67 +/- 0.12 mm [average]). Forty-nine deaths occurred over the median follow-up period of 24 months (interquartile range 10 to 34). Patients in the lowest tertile group of BAR (<2%) had significantly more events than those in the combined group of highest and mid-tertiles (p = 0.029, log-rank test). However, mean IMT (rather than flow-mediated dilation) was the vascular factor independently associated with mortality, even in the subgroup (n = 271) with no coronary artery disease and low risk. CONCLUSIONS: Brachial artery reactivity is lower in patients with events, but is not an independent predictor of cardiovascular outcomes in this cohort of patients.

Arteriosclerosis↗
PubMed2004

Use of tissue Doppler imaging to facilitate the prediction of events in patients with abnormal left ventricular function by dobutamine echocardiography.

The extent of abnormality in patients with positive dobutamine echocardiography (DE) is predictive of risk, but the wall motion score (WMS) has low concordance among observers. We sought whether quantifying the extent of abnormal wall motion using tissue Doppler (TD) could guide risk assessment in patients with abnormal DE in 576 patients with known or suspected coronary artery disease; standard DE was combined with color TD imaging at peak dose. WMS was assessed by an expert observer and studies were identified as abnormal in the presence of >/=1 segments with resting or stress-induced wall motion abnormalities. Patients with abnormal DE had peak systolic velocity measured in each segment. Tissue tracking was used to measure myocardial displacement. Follow-up for death or infarction was performed after 16 +/- 12 months. Of 251 patients with abnormal DE, 22 patients died (20 from cardiac causes) and 7 had nonfatal myocardial infarctions. The average WMS in patients with events was 1.8 +/- 0.5, compared with 1.7 +/- 0.5 in patients without events (p = NS). The average systolic velocity in patients with events was 4.9 +/- 1.7 cm/s and 6.4 +/- 6.5 cm/s in the patients without events (p <0.001). The average tissue tracking in patients with events was 4.5 +/- 1.5 mm and was significant (5.7 +/- 3.1 mm) in those without events (p <0.001). Thus, TD is an alternative to WMS for quantifying the total extent of abnormal left ventricular function at DE, and appears to be superior for predicting adverse outcomes.

Coronary Disease↗
PubMed2004

Postsystolic thickening detected by Doppler myocardial imaging: a marker of viability or ischemia in patients with myocardial infarction.

BACKGROUND: Postsystolic thickening (PST) of ischemic myocardial segments has been reported to account for the characteristic heterogeneity or regional asynchrony of myocardial wall motion during acute ischemia. HYPOTHESIS: Postsystolic thickening detected by Doppler myocardial imaging (DMI) could be a useful clinical index of myocardial viability or peri-infarction viability in patients with myocardial infarction (MI). METHODS: Doppler myocardial imaging was recorded at each stage of a standard dobutamine stress echocardiogram (DSE) in 20 patients (16 male, 60 +/- 13 years) with an MI in the territory of the left anterior descending artery. Myocardial velocity data were measured in the interventricular septum and apical inferior segment of the MI territory. Postsystolic thickening was identified if the absolute velocity of PST was higher than peak systolic velocity in the presence of either a resting PST > 2.0 cm/s or if PST doubled at low-dose dobutamine infusion. RESULTS: Doppler myocardial imaging data could be analyzed in 38 ischemic segments (95%), and PST was observed in 21 segments (55%), including 3 segments showing PST only at low-dose dobutamine infusion. There was no significant difference of baseline wall motion score index (2.1 +/- 0.3 vs. 2.1 +/- 0.6, p = 0.77) or peak systolic velocity (1.1 +/- 1.1 vs. 1.9 +/- 2.0 cm/s, p = 0.05) between segments with and without PST. Peri-infarction ischemia or viability during DSE was more frequently observed in segments with PST than in those without (86 vs. 24%, p < 0.05). The sensitivity and specificity of PST for prediction of peri-infarction viability or ischemia was 82 and 81%, respectively. CONCLUSIONS: Postsystolic thickening in the infarct territory detected by DMI is closely related with peri-infarction ischemia or viability at DSE.

Cardiotonic Agents↗
PubMed2004

Response of B-type natriuretic peptide to exercise in hypertensive patients with suspected diastolic heart failure: correlation with cardiac function, hemodynamics, and workload.

BACKGROUND: Diastolic heart failure (DHF) is characterized by dyspnea due to increased left ventricular (LV) filling pressures during stress. We sought the relationship of exercise-induced increases in B-type natriuretic peptide (BNP) to LV filling pressures and parameters of cardiovascular performance in suspected DHF. METHODS: Twenty-six treated hypertensive patients with suspected DHF (exertional dyspnea, LV ejection fraction >50%, and diastolic dysfunction) underwent maximal exercise echocardiography using the Bruce protocol. BNP, transmitral Doppler, and tissue Doppler for systolic (Sa) and early (Ea) and late (Aa) diastolic mitral annular velocities were obtained at rest and peak stress. LV filling pressures were estimated with E/Ea ratios. RESULTS: Resting BNP correlated with resting pulse pressure (r=0.45, P=0.02). Maximal exercise performance (4.6 +/- 2.5min) was limited by dyspnea. Blood pressure increased with exercise (from 143 +/- 19/88 +/- 8 to 191 +/- 22/ 90 +/- 10 mm Hg); 13 patients (50%) had a hypertensive response. Peak exercise BNP correlated with peak transmitral E velocity (r = 0.41, P <.05) and peak heart rate (r = -0.40, P <.05). BNP increased with exercise (from 48 +/- 57 to 74 +/- 97 pg/mL, P =.007), and the increment of BNP with exercise was associated with maximal workload and peak exercise Sa, Ea, and Aa (P <.01 for all). Filling pressures, approximated by lateral E/Ea ratio, increased with exercise (7.7 +/- 2.0 to 10.0 +/- 4.8, P <.01). BNP was higher in patients with possibly elevated filling pressures at peak exercise (E/Ea >10) compared to those with normal pressures (123 +/- 124 vs 45 +/- 71 pg/mL, P =.027). CONCLUSIONS: Augmentation of BNP with exercise in hypertensive patients with suspected DHF is associated with better exercise capacity, LV systolic and diastolic function, and left atrial function. Peak exercise BNP levels may identify exercise-induced elevation of filling pressures in DHF.

Atrial Function, Left↗
PubMed2004

Noninvasive tests for arterial structure, function, and compliance: do they identify risk or diagnose disease?

BACKGROUND: Brachial artery reactivity (BAR), carotid intima-media thickness (IMT), and applanation tonometry for evaluation of total arterial compliance may provide information about preclinical vascular disease. We sought to determine whether these tests could be used to identify patients with coronary artery disease (CAD) without being influenced by their ability to identify those at risk for CAD developing. METHODS: We studied 100 patients and compared 3 groups: 35 patients with known CAD; 34 patients with symptoms and risk factors but no CAD identified by stress echocardiography (risk group); and 31 control subjects. BAR and IMT were measured using standard methods, and total arterial compliance was calculated by the pulse-pressure method from simultaneous radial applanation tonometry and pulsed wave Doppler of the left ventricular outflow. Ischemia was identified as a new or worsening wall-motion abnormality induced by stress. RESULTS: In a comparison between the control subjects and patients either at risk for developing CAD or with CAD, the predictors of risk for CAD were: age (P =.01); smoking history (P =.002); hypercholesterolemia (P =.002); and hypertension (P =.004) (model R = 0.82; P =.0001). The independent predictors of CAD were: IMT (P =.001); BAR (P =.04); sex (P =.005); and hypertension (P =.005) (model R = 0.80; P =.0001). CONCLUSION: IMT, BAR, and traditional cardiovascular risk factors appear to identify patients at risk for CAD developing. However, only IMT was significantly different between patients at risk for developing CAD and those with overt CAD.

Aged↗
PubMed2004

Is quantitative interpretation likely to increase sensitivity of dobutamine stress echocardiography? A study of false-negative results.

BACKGROUND: False-negative interpretations of dobutamine stress echocardiography (DSE) may be associated with reduced wall stress. Using measurements of contraction, we sought whether these segments were actually ischemic but unrecognized or showed normal contraction. METHODS: We studied 48 patients (29 men; mean age 60 +/- 10 years) with normal regional function on the basis of standard qualitative interpretation of DSE. At coronary angiography within 6 months of DSE, 32 were identified as having true-negative and 16 as having false-negative results of DSE. Three apical views were used to measure regional function with color Doppler tissue, integrated backscatter, and strain rate imaging. Cyclic variation of integrated backscatter was measured in 16 segments, and strain rate and peak systolic strain was calculated in 6 walls at rest and peak stress. RESULTS: Segments with false-negative results of DSE were divided into 2 groups with and without low wall stress according to previously published cut-off values. Age, sex, left ventricular mass, left ventricular geometric pattern, and peak workload were not significantly different between patients with true- and false-negative results of DSE. Importantly, no significant differences in cyclic variation and strain parameters at rest and peak stress were found among segments with true- and false-negative results of DSE with and without low wall stress. Stenosis severity had no influence on cyclic variation and strain parameters at peak stress. CONCLUSIONS: False-negative results of DSE reflect lack of ischemia rather than underinterpretation of regional left ventricular function. Quantitative markers are unlikely to increase the sensitivity of DSE.

Coronary Angiography↗
PubMed2004

Quantitative assessment of aortic sclerosis using ultrasonic backscatter.

BACKGROUND: The development of therapeutic interventions to prevent progressive valve damage is more likely to limit the progression of structural damage to the aortic valve with normal function (aortic sclerosis [ASC]) than clinically apparent aortic stenosis. Currently, the ability to appreciate the progression of ASC is compromised by the subjective and qualitative evaluation of sclerosis severity. METHODS: We sought to reveal whether the intensity of ultrasonic backscatter could be used to quantify sclerosis severity in 26 patients with ASC and 23 healthy young adults. Images of the aortic valve were obtained in the parasternal long-axis view and saved in raw data format. Six square-shaped 11 x 11 pixel regions of interest were placed on the anterior and posterior leaflets, and calibrated backscatter values were obtained by subtracting the regions of interest in the blood pool from the averaged backscatter values obtained from the leaflets. RESULTS: Mean ultrasonic backscatter values for sclerotic valves exceeded the results in normal valve tissue (16.3 +/- 4.4 dB vs 9.8 +/- 3.3 dB, P < .0001). Backscatter values were greater (22.0 +/- 3.5 dB) in a group of 6 patients with aortic stenosis. Within the sclerosis group, the magnitude of backscatter was directly correlated (P < .05) with a subjective sclerosis score, and with transvalvular pressure gradient. Mean reproducibility was 2.4 +/- 1.8 dB (SD) between observers, and 2.3 +/- 1.7 dB (SD) between examinations. CONCLUSION: Measurement of backscatter from the valve leaflets of patients with ASC may be a feasible means of following the progression and treatment response of aortic sclerosis.

Aged↗
PubMed2004

Optimisation of strain rate imaging for application to stress echocardiography.

We sought to improve the feasibility of strain rate imaging (SRI) during dobutamine stress echocardiography (DSE) in 56 subjects at low risk of coronary disease. The impact of several SRI changes during acquisition were studied, including: (1) changing from fundamental to harmonic imaging; (2) parallel beamforming; (3) alteration of spatial resolution and (4) narrow sector acquisition. We assessed SR signal quality, a quantitative measure of signal noise and measurements of SRI. Of 1462 segments evaluated, 6% were uninterpretable at rest and 8% at peak stress. Signal quality was optimised by increasing temporal (p = 0.01) and spatial resolution (p < 0.0001 vs. baseline imaging) at rest and peak. Increasing spatial resolution also minimised signal noise (p < 0.0001). Inter-observer variability of time to peak SR and peak SR were less with high temporal and spatial resolution. SRI quality can be improved with harmonic imaging and higher temporal resolution but optimisation of spatial resolution is critical.

Cardiotonic Agents↗
PubMed2004

Effects of revascularisation and contractile reserve on left ventricular remodelling in patients with impaired left ventricular function.

OBJECTIVE: We sought to define the influence of revascularisation and contractile reserve on left ventricular (LV) remodelling in patients with LV dysfunction after myocardial infarction. Revascularisation of viable myocardium is associated with improved regional function, but the effect on remodelling is undefined. METHODS: We studied 70 patients with coronary artery disease and LV dysfunction, 31 of whom underwent revascularisation. A standard dobutamine stress echocardiogram (DbE) was carried out. All patients underwent standard medical treatment; the decision to revascularise was made clinically, independent of this study. LV volumes and ejection fraction were measured by 3D echocardiography at baseline and after an average of 40 weeks. RESULTS: There was no significant difference in baseline ejection fraction or volumes between patients who underwent revascularisation and the remainder. Compared to medically treated patients, revascularised patients had significant improvements in ejection fraction and end-systolic volume in follow-up. The impact of baseline variables on remodelling was assessed by dividing patients into tertiles of LV ejection fraction and volumes. Revascularised patients in the lowest tertile of ejection fraction at baseline (<38%) had a significant improvement in end-systolic volume and ejection fraction, larger than obtained in medically treated patients with low ejection fraction. Revascularised patients with an ejection fraction >38% did not show significant improvement in volumes compared to baseline. Revascularised patients in the largest tertiles of end-systolic (>88 ml) or end-diastolic volume (>149 ml) at baseline had a significant improvement in end-systolic volume. CONCLUSION: Remodeling appears to occur independent of the presence of regional contractile reserve but does correlate with the volume response to low-dose dobutamine.

Coronary Disease↗
PubMed2004

Relationship between longitudinal and radial contractility in subclinical diabetic heart disease.

Subclinical left ventricular (LV) dysfunction may be identified by reduced longitudinal contraction. We sought to define the effects of subclinical LV dysfunction on radial contractility in 53 patients with diabetes mellitus with no LV hypertrophy, normal ejection fraction and no ischaemia as assessed by dobutamine echocardiography, in comparison with age-matched controls. Radial peak myocardial systolic velocity (Sm) and early diastolic velocity (Em), strain and strain rate were measured in the mid-posterior and mid-anteroseptal walls in parasternal views and each variable was averaged for individual patients (radial contractility). These variables were also measured in the mid-posterior and mid-anteroseptal walls in the apical long-axis view and each variable was averaged for individual patients (longitudinal contractility). Mean radial Sm, strain and strain rate were significantly increased in diabetic patients (2.9 +/- 0.6 cm/s, 28 +/- 5% and 1.8 +/- 0.4 s(-1) respectively) compared with controls (2.4 +/- 0.7 cm/s, 23 +/- 4% and 1.6 +/- 0.3 s(-1) respectively; all P<0.001), but there was no difference in Em (3.3 +/- 1.2 compared with 3.1 +/- 1.1 cm/s, P=not significant). In contrast, longitudinal Sm, Em, strain and strain rate were significantly lower in diabetic patients (3.6 +/- 1.1 cm/s, 4.3 +/- 1.6 cm/s, 21 +/- 4% and 1.6 +/- 0.3 s(-1) respectively) than in controls (4.3 +/- 1.0 cm/s, 5.7 +/- 2.3 cm/s, 26 +/- 4% and 1.9 +/- 0.3 s(-1) respectively; all P< or =0.001). Thus radial contractility appears to compensate for reduced longitudinal contractility in subclinical LV dysfunction occurring in the absence of ischaemia or LV hypertrophy.

Adult↗
PubMed2004

The effect of long-term aggressive lipid lowering on ischemic and atherosclerotic burden in patients with chronic kidney disease.

BACKGROUND: Cardiac mortality is the main cause of death in patients with chronic kidney disease (CKD). In this study, we sought the efficacy of long-term intensive lipid level lowering on atherosclerotic burden in patients with CKD. METHODS: Patients with CKD (n = 38; age, 64 +/- 11 years) and a similar group of patients with coronary artery disease (CAD; n = 31) were treated prospectively with atorvastatin, up to 80 mg/d. Lipid profile, carotid intima-media thickness (IMT; a marker of atherosclerotic burden), and dobutamine echocardiography were measured at baseline and 2 years. Predictors of change in maximal IMT were sought in a linear model. RESULTS: Despite similar cholesterol level lowering, patients with CAD showed an improvement in maximum IMT, whereas those with CKD did not (mean between-group difference, 0.07 mm; 95% confidence interval, 0.01 to 0.12). Change in maximal IMT was associated with kidney disease (R2 = 0.09; P = 0.013), smoking (R2 = 0.083; P = 0.017), baseline low-density lipoprotein cholesterol (LDL-C) level (R2 = 0.064; P = 0.045), very low density cholesterol (VLDL-C) level (R2 = 0.084; P = 0.021), and calcium channel blocker use (R2 = 0.094; P = 0.01). In a multivariate model, kidney disease and baseline LDL-C and VLDL-C levels remained independent predictors of change in maximal IMT (model R2 = 0.24; P = 0.004). Only patients with CAD decreased their number of ischemic segments (2.5 +/- 1.4 to 1.2 +/- 1.5 segments; P = 0.002). Overall change in ischemic segment number correlated with change in maximal IMT (r = 0.32; P = 0.019). CONCLUSION: Patients with CKD undergoing intensive lipid level lowering do not show the same changes in atherosclerotic or ischemic burden as patients with CAD. Independent predictors of change in maximal IMT were CKD and baseline LDL-C and VLDL-C levels.

Aged↗
PubMed2004

Tissue Doppler imaging for evaluation of myocardial function in patients with diabetes mellitus.

PURPOSE OF REVIEW: Heart failure and diabetes mellitus are frequently associated, and diabetes appears to potentiate the clinical presentation of heart failure related to other causes. The purpose of this review is to examine recent advances in the application of tissue Doppler imaging for the assessment of diabetic heart disease. RECENT FINDINGS: Recent studies have documented that both myocardial systolic and diastolic abnormalities can be identified in apparently healthy patients with diabetes and no overt cardiac dysfunction. Interestingly, these are disturbances of longitudinal function, with compensatory increases of radial function-suggesting primary involvement of the subendocardium, which is a hallmark of myocardial ischemia. Despite this, there is limited evidence that diabetic microangiopathy is responsible-with reduced myocardial blood volume rather than reduced resting flow, and at least some evidence suggesting a normal increment of tissue velocity with stress. Finally, a few correlative studies have shown association of diabetic myocardial disease with poor glycemic control, while angiotensin converting enzyme inhibition may be protective. SUMMARY: Tissue Doppler imaging (and the related technique of strain rate imaging) appears to be extremely effective for the identification of subclinical LV dysfunction in diabetic patients. It is hoped that the recognition of this condition will prompt specific therapy to prevent the development of overt LV dysfunction.

Diabetes Mellitus↗
PubMed2004

Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications.

The presence of a diabetic cardiomyopathy, independent of hypertension and coronary artery disease, is still controversial. This systematic review seeks to evaluate the evidence for the existence of this condition, to clarify the possible mechanisms responsible, and to consider possible therapeutic implications. The existence of a diabetic cardiomyopathy is supported by epidemiological findings showing the association of diabetes with heart failure; clinical studies confirming the association of diabetes with left ventricular dysfunction independent of hypertension, coronary artery disease, and other heart disease; and experimental evidence of myocardial structural and functional changes. The most important mechanisms of diabetic cardiomyopathy are metabolic disturbances (depletion of glucose transporter 4, increased free fatty acids, carnitine deficiency, changes in calcium homeostasis), myocardial fibrosis (association with increases in angiotensin II, IGF-I, and inflammatory cytokines), small vessel disease (microangiopathy, impaired coronary flow reserve, and endothelial dysfunction), cardiac autonomic neuropathy (denervation and alterations in myocardial catecholamine levels), and insulin resistance (hyperinsulinemia and reduced insulin sensitivity). This review presents evidence that diabetes is associated with a cardiomyopathy, independent of comorbid conditions, and that metabolic disturbances, myocardial fibrosis, small vessel disease, cardiac autonomic neuropathy, and insulin resistance may all contribute to the development of diabetic heart disease.

Animals↗