Search PubMed⌕ Search

Biomedical subjects

Josef Korinek

Publications and source records attributed to Josef Korinek.

12 recordsLinked to original sources
PubMed2006

Left ventricular structure and function: basic science for cardiac imaging.

The myofiber geometry of the left ventricle (LV) changes gradually from a right-handed helix in the subendocardium to a left-handed helix in the subepicardium. In this review, we associate the LV myofiber architecture with emerging concepts of the electromechanical sequence in a beating heart. We discuss: 1) the morphogenesis and anatomical arrangement of muscle fibers in the adult LV; 2) the sequence of depolarization and repolarization; 3) the physiological inhomogeneity of transmural myocardial mechanics and the apex-to-base sequence of longitudinal and circumferential deformation; 4) the sequence of LV rotation; and 5) the link between LV deformation and the intracavitary flow direction observed during each phase of the cardiac cycle. Integrating the LV structure with electrical activation and motion sequences observed in vivo provides an understanding about the spatiotemporal sequence of regional myocardial performance that is essential for noninvasive cardiac imaging.

Aging↗
PubMed2006

Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies.

BACKGROUND: Studies of the association between obesity, and total mortality and cardiovascular events in patients with coronary artery disease (CAD) have shown contradictory results. We undertook a systematic review to determine the extent and nature of this association. METHODS: We selected cohort studies that provided risk estimates for total mortality, with or without cardiovascular events, on the basis of bodyweight or obesity measures in patients with CAD, and with at least 6 months' follow-up. CAD was defined as history of percutaneous coronary intervention, coronary artery bypass graft, or myocardial infarction. We obtained risk estimates for five predetermined bodyweight groups: low, normal weight (reference), overweight, obese, and severely obese. FINDINGS: We found 40 studies with 250,152 patients that had a mean follow-up of 3.8 years. Patients with a low body-mass index (BMI) (ie, <20) had an increased relative risk (RR) for total mortality (RR=1.37 [95% CI 1.32-1.43), and cardiovascular mortality (1.45 [1.16-1.81]), overweight (BMI 25-29.9) had the lowest risk for total mortality (0.87 [0.81-0.94]) and cardiovascular mortality (0.88 [0.75-1.02]) compared with those for people with a normal BMI. Obese patients (BMI 30-35) had no increased risk for total mortality (0.93 [0.85-1.03]) or cardiovascular mortality (0.97 [0.82-1.15]). Patients with severe obesity (> or =35) did not have increased total mortality (1.10 [0.87-1.41]) but they had the highest risk for cardiovascular mortality (1.88 [1.05-3.34]). INTERPRETATION: The better outcomes for cardiovascular and total mortality seen in the overweight and mildly obese groups could not be explained by adjustment for confounding factors. These findings could be explained by the lack of discriminatory power of BMI to differentiate between body fat and lean mass.

Angioplasty, Balloon, Coronary↗
PubMed2006

Accuracy, reproducibility, and comparability of Doppler tissue imaging by two high-end ultrasound systems.

INTRODUCTION: Doppler tissue imaging is a new technology for quantitative evaluation of myocardial motion and contractility, and is available in several ultrasound systems. This study evaluates the comparability, accuracy, and reproducibility of measurements of velocity, strain rate, and strain by two high-end ultrasound systems. METHODS: Accuracy was assessed by imaging a tissue-mimicking gelatin phantom, and the comparability of measurements in the right ventricular free wall and interventricular septum was assessed in 20 healthy participants. Reproducibility was evaluated by repeated recordings in vitro and in a random subset of patients. RESULTS: In vitro, a high degree of accuracy was found in both systems, with one system measuring slightly lower values than the reference values (mean difference 0.35 +/- 0.18 cm/s, P < .001). Values higher than the reference values were measured by both systems for strain and strain rate. In vivo, no systematic differences in measured velocities, strain rate, and strain were found; however, wide limits of agreement were seen for strain and strain rate. Measurements of tissue velocity, strain, and strain rate were well reproducible, nevertheless wide variation was found in both systems (coefficient of variation = 9%-19%). CONCLUSION: For clinical purposes, both systems have sufficient accuracy for measurements of tissue velocity. The variation in measurements of strain rate and strain by Doppler tissue imaging should be taken into account when designing studies using this new technology. Approaches to potentially reduce this variation should be addressed in future studies.

Echocardiography, Doppler↗
PubMed2006

Analysis of postsystolic myocardial thickening work in selective myocardial layers during progressive myocardial ischemia.

BACKGROUND: Myocardial function is transmurally heterogeneous. Postsystolic work may functionally reflect ischemic but viable myocardium. We calculated systolic and postsystolic regional myocardial work index (RMWi) in subendocardial and subepicardial layers of myocardium supplied by a slowly occluding coronary artery. METHODS: Progressive stenosis of the left anterior descending coronary artery lasting 11 +/- 5 days (end point) was induced in 10 dogs, and pressure-strain loops were obtained from subendocardial and subepicardial layers of apical and middle anterior segments by intracardiac ultrasound. RESULTS: At baseline, the RMWi was significantly higher (P < .05) in the subendocardial layer. At the end point, there was no significant change in the RMWi in ischemic myocardium; however, the postsystolic RMWi was higher (P < .05) in the subendocardial layer and accompanied a decrease in subendocardial myocardial blood flow, although viability was largely maintained. CONCLUSION: A significant subendocardial postsystolic RMWi at rest suggests an impending ischemic injury in coronary artery disease when segmental function is still preserved.

Animals↗
PubMed2005

Apex-to-base dispersion in regional timing of left ventricular shortening and lengthening.

OBJECTIVES: We investigated whether the onset and progression of regional left ventricular (LV) shortening and lengthening parallel the apex-to-base differences in depolarization and repolarization. BACKGROUND: Limited information exists regarding apex-to-base differences in longitudinal and circumferential deformation sequence of the LV. METHODS: The apex-to-base differences in electric activation and the progression of longitudinal and circumferential shortening and lengthening sequences were determined in 8 porcine beating hearts in situ by implanting bipolar electrodes and an array of 14 sonomicrometry crystals in the LV free wall. RESULTS: Electric activation started at the apical subendocardium and showed significant delay in reaching the LV base. The onsets of mechanical activation and subsequent 20%, 40%, and 80% peak longitudinal shortenings required longer time to occur at base compared to the apex. The repolarization sequence propagated in reverse, with the base repolarizing before the apex. Subendocardial longitudinal shortening at base and subepicardial circumferential shortening at apex continued beyond the period of LV ejection, resulting in an apex-to-base gradient in the onset of lengthening. This gradient correlated with the duration of isovolumic relaxation (r = 0.85, p = 0.004) and the time required for reaching the lowest LV diastolic pressure (r = 0.70, p = 0.04). CONCLUSIONS: Apex-to-base delay in mechanical shortening of LV parallels the apex-to-base direction of the electric activation sequence. Basal subendocardial and apical subepicardial regions deform through a characteristic phase of postsystolic shortening. Short-lived apex-to-base and subendocardial-to-subepicardial relaxation gradients at the onset of diastole may have a physiologic significance in facilitating active restoration of the LV cavity in diastole.

Animals↗
PubMed2005

Delayed onset of subendocardial diastolic thinning at rest identifies hypoperfused myocardium.

BACKGROUND: Onset of myocardial relaxation is highly energy dependent. Perfusion and therefore energy substrate delivery are predominantly reduced in the subendocardial myocardium in the early stages of progressive ischemia. We hypothesized that delayed onset of subendocardial diastolic thinning will functionally identify regionally hypoperfused resting myocardium. METHODS AND RESULTS: Progressive left anterior descending coronary artery stenosis was induced by an ameroid occluder and maintained for 1 or 2 weeks (end point) in 12 dogs. M-mode tissue Doppler images of the anterior apical and middle segments (testing region) and middle inferior segment (control region) were acquired selectively in the subendocardium and subepicardium. The time to the onset of thinning was measured with the use of tissue Doppler velocity (TOTv) and a thickness function (TOTt). At the end point in the testing region, myocardial flow was significantly lower in the subendocardial layer (P<0.05) in all animals, whereas viability staining showed preserved transmural viability in 10 dogs and thin subendocardial necrosis in 2 dogs. Both TOTv and TOTt were significantly (P<0.01) prolonged in the testing region. The mean difference between subendocardial and subepicardial TOTv values versus that in the control region identified the ischemic region, even when only dogs with hypoperfused but transmurally viable myocardium were considered (P<0.05). Systolic and diastolic myocardial velocities did not identify subendocardial hypoperfusion. CONCLUSIONS: In resting myocardium subtended to progressive coronary stenosis, a delayed onset of subendocardial thinning suggests an early stage of hypoperfusion, before the development of local wall motion abnormalities.

Animals↗
PubMed2005

Biphasic tissue Doppler waveforms during isovolumic phases are associated with asynchronous deformation of subendocardial and subepicardial layers.

Subendocardial and subepicardial layers of the left ventricle (LV) are characterized with right- and left-handed helical orientations of myocardial fibers. We investigated the origin of biphasic deformations of the LV wall during isovolumic contraction (IVC) and relaxation (IVR). In eight open-chest adult pigs, strain rates were measured along the right- and left-handed helical directions in the LV anterior wall by implanting 16 sonomicrometry crystals. Sonomicrometry strain rates were compared with the longitudinal subendocardial strain rates obtained by tissue Doppler imaging. During ejection and diastolic filling, shortening and lengthening occurred synchronously along the right- and left-handed helical directions. However, during IVC and IVR, the deformations were dissimilar in the two directions. Transmural shortening during IVC occurred along the right-handed helical direction and was accompanied with transient lengthening in the left-handed helical direction. Conversely, during IVR, the LV lengthened along the left-handed helical direction and shortened in the right-handed helical direction. Peak subendocardial strain rates obtained by tissue Doppler imaging during IVC and IVR correlated with corresponding sonomicrometry strain rate values obtained along the right- and left-handed helical directions (r = 0.81, P < 0.001 and r = 0.70, P = 0.001, respectively). Our data suggest that brief counterdirectional movements occur within the LV wall during IVC and IVR. Shortening along the right-handed helical direction is accompanied with reciprocal lengthening in the left-handed helical direction during IVC and vice versa during IVR. The results support an association between asynchronous deformation of subendocardial and subepicardial muscle fibers and the biphasic isovolumic movements observed with high-resolution tissue Doppler imaging.

Animals↗
PubMed2005

Increased right ventricular afterload induces postsystolic thickening of the ventricular septum in nonischemic hearts.

BACKGROUND: We aimed to assess whether myocardial postsystolic thickening (PST) can be induced by an acute increase in right ventricular (RV) afterload and, thus, demonstrate that PST may have a nonischemic cause. METHODS: In 8 anesthetized open-chest pigs, radial strains of the interventricular septum (IVS) and left ventricular inferolateral wall were obtained by Doppler tissue echocardiography before and during constriction of the pulmonary artery. RESULTS: After each constriction, RV peak systolic pressure increased from 30 +/- 5 to 57 +/- 8 mm Hg (P < .001). Peak systolic radial strain of the IVS decreased from 20.8% +/- 5.3% to 9.5% +/- 4.1% (P = .003), and PST of the IVS increased from 0.3% +/- 0.5% to 6.1% +/- 4.8% (P = .01). The onset of PST started 41 +/- 20 milliseconds after peak negative dP/dt of RV pressure. The inferolateral wall did not show PST. CONCLUSION: An acute increase in RV pressure causes a significant reduction in peak systolic strain of the IVS associated with the nonischemic appearance of PST.

Animals↗
PubMed2005

Two-dimensional strain--a Doppler-independent ultrasound method for quantitation of regional deformation: validation in vitro and in vivo.

BACKGROUND: A new 2-dimensional strain echocardiography (2DSE) method has been introduced that measures myocardial deformations by tracking localized acoustic markers. We compared strains measured in vitro and in vivo by 2DSE with those obtained by sonomicrometry. METHODS: For the in vitro study, a tissue-mimicking gelatin block was cyclically compressed and longitudinal strains obtained by 2DSE and sonomicrometry crystals. For the in vivo study, arrays of crystals were implanted into the apical anteroseptal (test region) and midposterior (control region) in 16 open-chest pigs and strains measured by 2DSE and crystals at baseline and after acute ischemia. RESULTS: In vitro, pooled data demonstrated good correlation (r = 0.99, P < .0001) and close agreement (bias +/- 2SD = 0.7 +/- 2.2%) of 2DSE and sonomicrometry. For a combination of low testing strains (5.4%) and strain rates (0.8 and 1.2 Hz), 2DSE overestimated strains by sonomicrometry. In vivo, linear regression analysis of pooled measurements demonstrated again a good correlation (r = 0.94, P < .0001) and agreement (1.1 +/- 7.5%) of 2DSE with sonomicrometry with a trend toward lower absolute values of strains by 2DSE. CONCLUSION: The 2DSE demonstrated good overall correlation and agreement with sonomicrometry for the tested in vitro and in vivo values. Some caution with 2DSE measurements is needed for combinations of low strains and strain rates.

Animals↗
PubMed2004

Both systolic and diastolic dysfunction characterize nonischemic inhibition of myocardial energy metabolism: an experimental strain rate echocardiographic study.

BACKGROUND: Ischemia is primarily a metabolic event. However, regional functional changes can be affected by structural alterations. We developed an experimental model of sole myocardial energy metabolism inhibition and characterized the resulting regional dysfunction. METHODS: In 12 pigs, we regionally inhibited creatine kinase (CK) and, consequently, myocyte high-energy phosphate transfer by intracoronary administration of iodoacetamide. Myocardial biopsies for CK activity and structural analyses and strain rate (SR) echocardiography scans were obtained at baseline and 60 minutes after iodoacetamide administration. Plasma levels of the CK isoenzyme MB and troponin I were assessed to determine possible myocardial damage. RESULTS: CK activity in the iodoacetamide-perfused myocardium decreased to 0.5% of the original value and was accompanied by a reduction in peak systolic SR ( P < .0001), end-systolic strain ( P < .0001), and peak SRs of myocardial early and late filling waves ( P < .0001). Microscopy showed contracture without sarcomere disruption. Plasma levels of CK isoenzyme MB and troponin I did not change. CONCLUSIONS: Regional inhibition of myocyte energetics leads to both systolic and diastolic dysfunction by SR echocardiography, but the presence of a residual phosphotransfer protects microstructural integrity.

Animals↗
PubMedDate not supplied

Update in prevention of atherosclerotic heart disease: management of major cardiovascular risk factors.

Cardiovascular disease (CVD) remains as the first cause of death worldwide. Scientific community works everyday trying to ameliorate this burden. Only in the year 2004 around 2,790 publications about the therapeutic use of antihypertensive agents can be found in MEDLINE. Despite this overwhelming effort and information, only a relatively short number of manuscripts have a real impact in clinical practice. For the busy clinician, it becomes almost impossible to screen and be updated with the landmark publications. The purpose of this article is to provide concise information related to prevention of CVD. We reviewed publications in the past 5 years regarding cardiovascular risk factors with special attention to dyslipidemia, hypertension, diabetes, smoking cessation and obesity, discussing some new findings and treatments. We also discuss obstructive sleep apnea (OSA) as a recently identified cardiovascular risk factor, and provide a general overview about its pathophysiology and treatment.

Antihypertensive Agents↗