Search PubMed⌕ Search

Biomedical subjects

Petri Sipola

Publications and source records attributed to Petri Sipola.

7 recordsLinked to original sources

Characterization and molecular detection of atherothrombosis by magnetic resonance--potential tools for individual risk assessment and diagnostics.

This review focuses on recent non-invasive or minimally invasive magnetic resonance (MR) approaches to study atherothrombosis. The potential benefits of combining diverse metabolic information obtained by the variety of MR techniques from tissues in vivo and ex vivo and from body fluids in vitro are also briefly discussed. A well established methodology is available for lipoprotein subclass quantification from plasma by 1H MR spectroscopy providing information for assessing the long-term risk of atherosclerosis. Multi-contrast MR imaging in vivo relying on endogenous contrast allows partial characterization of components in atherothrombotic plaques. The use of exogenous contrast agents in MR angiography enhances blood-tissue contrast and provides functional information on plaque metabolism, improving plaque characterization and assessment of plaque vulnerability by MR imaging. Recent applications of molecular targeted MR imaging have revealed novel opportunities for specific early detection of atherothrombotic processes, such as angiogenesis and accumulation of macrophages. Currently, MR imaging and spectroscopy can produce such metabolic in vivo and in vitro information that in combination could facilitate the screening, identification and follow-up of cardiovascularly vulnerable patients in research settings. The recent developments imply that in the near future MR techniques will be part of clinical protocols for individual diagnostics in atherothrombosis.

Animals↗

Cine MR imaging of myocardial contractile impairment in patients with hypertrophic cardiomyopathy attributable to Asp175Asn mutation in the alpha-tropomyosin gene.

PURPOSE: To prospectively investigate the relationship between myocardial contractile impairment and left ventricular (LV) hypertrophy measured at cardiac magnetic resonance (MR) imaging in patients with hypertrophic cardiomyopathy (HCM) caused by the substitution of aspartic acid 175 with asparagine (ie, Asp175Asn mutation) in the alpha-tropomyosin gene (TPM1). MATERIALS AND METHODS: The study protocol was approved by the hospital ethics committee, and all subjects gave written informed consent. LV mass, maximal LV wall thickness, and myocardial fractional thickening during systole were measured at cine MR imaging in 24 subjects (11 male, 13 female; mean age, 42 years; age range, 17-68 years) with the Asp175Asn mutation in TPM1 and in 17 healthy volunteers (eight men, nine women; mean age, 38 years; age range, 23-60 years). The proportion of hypokinetic LV segments was calculated as the number of LV segments with fractional thickening of less than 30% divided by the total number of segments measured. Anthropometric and biochemical correlates of LV hypertrophy were determined. Univariate and multiple linear regression analyses were used to investigate the association of the proportion of hypokinetic segments and other correlates of LV hypertrophy with LV mass and maximal wall thickness. RESULTS: The proportion of hypokinetic segments was higher in patients with HCM than in control subjects (37% +/- 20 [standard deviation] vs 12% +/- 12, P < .001). In stepwise multiple regression analysis, the proportion of hypokinetic segments accounted for 42% (P < .001); the LV end-diastolic volume, for 24% (P = .003); and male sex, for 10% (P = .014) of the variability in LV mass in patients with HCM. The proportion of hypokinetic LV segments, which accounted for 48% of the variability in LV maximal wall thickness (P < .001), was the only variable significantly associated with maximal wall thickness. CONCLUSION: The extent of myocardial contractile impairment is strongly and independently related to LV mass and maximal wall thickness in patients with HCM attributable to the Asp175Asn mutation in TPM1.

Adult↗

Repair of right ventricular free wall defect with a de-epithelized pedicled myocutaneous latissimus dorsi muscle flap.

Rupture of the right ventricle may occur because of sternal dehiscence or mediastinitis after cardiac surgery. Direct suture, polytetrafluoroethylene patch, fasciae, and muscle flaps have been used to close a right ventricular rupture. A unique occurrence of repair of a full-thickness right ventricle defect with a de-epithelized myocutaneous flap is presented. Our patient experienced a rupture of the right ventricle complicating sternal wound infection. The rupture was reconstructed with a polytetrafluoroethylene patch, but the patch needed to be removed because of infection. The defect was reconstructed with a de-epithelized myocutaneous latissimus dorsi flap. The patient indicated no signs of complication during follow-up.

Aged↗

Multi-detector row CT angiography in the assessment of carotid artery disease in symptomatic patients: comparison with rotational angiography and digital subtraction angiography.

BACKGROUND AND PURPOSE: Compared with the single-detector technique, multi-detector row CT angiography permits larger anatomic coverage that includes both the epiaortic and entire carotid circulations. We evaluated the accuracy of multi-detector row CT angiography by using multiplanar reformation (MPR) for measuring carotid artery diameters compared with that of rotational angiography. We also evaluated the diagnostic performance of CT angiography compared with digital subtraction angiography (DSA). METHODS: In 35 patients, CT angiograms of 70 carotid arteries were compared with DSA images, and CT angiograms of 33 carotid arteries were compared with rotational angiograms. CT angiographic interpretation was performed first interactively at a workstation. Diameter measurements of normal and stenosed carotid arteries were performed on cross-sectional and oblique sagittal MPRs. Degree of stenosis was calculated per North American Symptomatic Carotid Endarterectomy Trial criteria independently by two observers for each technique. RESULTS: Degree of stenosis was slightly underestimated with CT angiography, with mean differences (+/- SD) per observer of 6.9 +/- 17.6% and 10.7 +/- 16.1% for cross-sectional and 2.8 +/- 19.2% and 9.1 +/- 16.8% for oblique sagittal MPRs compared with rotational angiography. CT angiography was somewhat inaccurate for measuring the absolute minimal diameter of high-grade stenoses. On symptomatic sides (n = 35), interactive CT angiographic interpretation combined with MPR measurements for lesions with a visual estimate of 50% or greater stenosis achieved a sensitivity of 95% (20/21) and specificity of 93% (13/14) in the detection of carotid stenosis (>/= 50%) verified with DSA. CONCLUSION: Regardless of slight underestimation of carotid stenosis with CT angiography compared with rotational angiography, diagnostic performance of CT angiography with interactive interpretation proved to be good. Also, the method is highly sensitive for detection of carotid artery stenosis, indicating the suitability of CT angiography as a screening method for symptomatic patients. For hemodynamically significant stenoses revealed by CT angiographic screening, conventional angiography still seems to be necessary.

Aged↗

First-pass MR imaging in the assessment of perfusion impairment in patients with hypertrophic cardiomyopathy and the Asp175Asn mutation of the alpha-tropomyosin gene.

PURPOSE: To assess first-pass magnetic resonance (MR) imaging in the evaluation of perfusion impairment in a genetically homogeneous population of patients with hypertrophic cardiomyopathy (HCM) and the Asp175Asn mutation of the alpha-tropomyosin gene and to evaluate the association between hypertrophy and perfusion. MATERIALS AND METHODS: Rest-stress first-pass MR imaging with gadopentetate dimeglumine was performed in 17 patients with HCM and the Asp175Asn substitution in the alpha-tropomyosin gene and in five control subjects. Global and segmental first-pass reserve index (FPR) measurements were derived from signal intensity versus time curves. Left ventricular (LV) wall thickness and LV mass index were measured on cine MR images. The Mann-Whitney test was used to evaluate the difference in FPR between the patient group and the control group. The Spearman correlation was used to evaluate the association between LV hypertrophy and FPR. RESULTS: Global FPR was significantly lower in the patients with HCM than in the control subjects (1.12 +/- 0.35 vs 1.80 +/- 0.58, P =.015). In patients with HCM, maximal LV wall thickness and LV mass index correlated negatively with global FPR (r = -0.723, P =.001 and r = -0.598, P =.011, respectively). At the regional level, segmental FPR correlated inversely with LV wall thickness (r = -0.389; P <.001) in patients with HCM. CONCLUSION: First-pass MR imaging facilitates global and regional evaluation of perfusion impairment in patients with HCM. The severity of perfusion impairment is associated with the degree of LV hypertrophy.

Adenosine↗

Cardiac adrenergic activity is associated with left ventricular hypertrophy in genetically homogeneous subjects with hypertrophic cardiomyopathy.

UNLABELLED: Hypertrophic cardiomyopathy (HCM) is a genetic disease caused by mutations in genes encoding sarcomeric proteins. However, other genetic and possibly also environmental factors modify the phenotypic expression of left ventricular (LV) hypertrophy. The present study investigated whether cardiac adrenergic activity affects the severity of LV hypertrophy in genetically identical patients with HCM. METHODS: The study population consisted of 21 patients with HCM caused by the Asp175Asn substitution of the alpha-tropomyosin gene (TPM1-Asp175Asn) and 9 healthy volunteers. LV mass and segmental wall thickness were measured with MRI. Presynaptic cardiac adrenergic activity was measured with (123)I-metaiodobenzylguanidine (MIBG) SPECT. Global and segmental washouts of (123)I-MIBG were calculated. RESULTS: Global myocardial (123)I-MIBG washout was faster in patients with TPM1-Asp175Asn than in healthy volunteers (50% +/- 9% vs. 37% +/- 8%, P = 0.001). In linear regression analysis, global (123)I-MIBG washout was associated with the LV mass index and LV maximal wall thickness index in HCM patients (r = 0.512, P = 0.018, and r = 0.478, P = 0.028, respectively). The mean (123)I-MIBG washout was higher in LV segments >/= 15 mm thick than in LV segments < 15 mm thick (56 +/- 10 vs. 49% +/- 10%, P = 0.002). CONCLUSION: In patients with HCM sharing the same causal gene defect, the degree of LV hypertrophy is related to (123)I-MIBG washout, suggesting that cardiac adrenergic activity modifies phenotypic expression in HCM.

3-Iodobenzylguanidine↗