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Biomedical subjects

M Krzanowski

Publications and source records attributed to M Krzanowski.

At least 19 recordsLinked to original sources
PubMed2003

Genetic polymorphisms associated with acute pulmonary embolism and deep venous thrombosis.

Frequently an inherited predisposition to thrombosis remains clinically silent until an additional environmental factor intervenes. The present study aimed to assess distribution of inherited risk factors of venous thrombosis in patients with venous thromboembolism (VTE). The prevalences of factor V Leiden (FV Leiden), prothrombin factor II G20210A (FII G20210A), C677T and A1298C of methylenetetrahydrofolate reductase (MTHFR) mutations were studied in 149 VTE patients and 100 controls. The following key risks were established: previous deep venous thrombosis or pulmonary embolism (23.5%), bed rest (34.2%), immobilisation of lower limb (10.1%), hospitalisation (30.9%) and obesity (28.9%). In 29 (19%) patients and in three (3%) controls FV Leiden was found. A significant association between VTE and FV Leiden was established. There were six (4%) carriers of the FII G20210A among VTE patients and one in the controls. No associations between VTE and MTHFR polymorphisms (C677T, A1298C) were found. In three of 149 patients both FV Leiden and FII G20210A polymorphisms were observed. The mean protein C activity was slightly, though nonsignificantly, smaller in VTE patients. In conclusion, there was a positive association between venous thromboembolism and factor V Leiden. Only a weak trend favouring a relationship between prothrombin factor II G20210A and venous thrombolism was present. No associations between common polymorphisms of methylenetetrahydrofolate reductase and venous thromboembolism were found.

Case-Control Studies↗
PubMed2001

The effect of verapamil on response of coronary vasomotion to handgrip exercise in symptomatic patients with hypertrophic cardiomyopathy.

OBJECTIVES: To assess the effect of verapamil on the response of diastolic coronary blood flow velocity (CBFV) and coronary vascular resistance index to handgrip exercise in symptomatic HCM patients. DESIGN: In 13 patients with HCM, the CBFV was detected in the distal portion of left anterior descending coronary artery using high-sensitivity transthoracic Doppler echocardiography. The peak diastolic CBFV and coronary vascular resistance index (calculated as the ratio of mean aortic pressure to CBFV) was measured at baseline and during handgrip exercise. Changes of these parameters induced by the exercise (expressed as the percentage of baseline values) were compared on verapamil treatment and after verapamil withdrawal. The same measurements were obtained in 10 healthy control subject. RESULTS: In HCM patients, the increase in CBFV during exercise was significantly higher on than off verapamil therapy (16.2 +/- 5% versus 6.8 +/- 3.8%, p < 0.001). In healthy controls, exercise-induced increase in CBFV was comparable to CBFV changes in HCM patients receiving verapamil (17.4 +/- 5.7 versus 16.2 +/- 5%, p > 0.05) and was significantly greater than the CBFV response in HCM patients off verapamil (17.4 +/- 5.7% versus 6.8 +/- 3.8% p < 0.005). During exercise the coronary vascular resistance index decreased on verapamil and increased after drug withdrawal (-5.8 +/- 5.6% versus 1.1 +/- 5.1%, p < 0.001). In healthy controls the coronary vascular resistance index decreased during exercise -8.5 +/- 4.5% to similar extent as in HCM patients on verapamil. CONCLUSION: In HCM symptomatic patients, verapamil improved coronary vasomotor response to physical stress. Verapamil was able to restore adequate vasodilator response to handgrip exercise.

Adult↗
PubMed2000

Comparison of the effect of verapamil and propranolol on response of coronary vasomotion to cold pressor test in symptomatic patients with hypertrophic cardiomyopathy.

Impaired endothelium-dependent vasodilatation of coronary resistance vessels has been demonstrated in patients with hypertrophic cardiomyopathy (HC). The aim of this study was to compare the effect of verapamil and propranolol on the response of diastolic coronary blood flow velocity (CBFV) and coronary vascular resistance index to the cold pressor test (CPT) in symptomatic HC patients. In 15 patients with HC, the CBFV was measured in the distal portion of the left anterior descending coronary artery using high-sensitivity transthoracic Doppler echocardiography. Peak diastolic CBFV and coronary vascular resistance index (calculated as ratio of mean aortic pressure/CBFV ratio) were measured at baseline and after CPT. Changes of these parameters induced by the CPT (expressed as percentage of baseline values) were compared after verapamil and propranolol treatment in a crossover study. The same measurements were obtained in nine healthy control subjects. CPT induced an increasing pattern of CBFV during verapamil therapy, which was absent in CPT after propranolol administration (10.1 +/- 5.6% vs. -0.9 +/- 4.1%, P < 0.01). In healthy controls CBFV increased in response to CPT more than in HC patients receiving verapamil or propranolol (23.1+/- 12.8% P < 0.01 and P < 0.05, respectively). The coronary vascular resistance index increased during the CPT significantly less on verapamil than on propranolol treatment (3.5 +/- 9.2% vs. 18.1 +/- 13.5%, P < 0.01). In healthy controls the coronary vascular resistance index decreased during CPT -4.5 +/- 8.5% (P < 0.05 vs. verapamil and P < 0.01 vs. propranolol). Verapamil improved the coronary vasomotor response to CPT in relation to propranolol. Verapamil blunted the increase of the coronary vascular resistance index to the CPT in comparison with its change at CPT after propranolol. Thus, coronary endothelial dysfunction in symptomatic HC patients may be partially reduced by verapamil in comparison with propranolol treatment.

Adrenergic beta-Antagonists↗
PubMed2000

Value of transthoracic echocardiography for the detection of high-grade coronary artery stenosis: prospective evaluation in 50 consecutive patients scheduled for coronary angiography.

We prospectively evaluated the feasibility of direct, transthoracic evaluation of coronary arteries to diagnose flow-limiting lesions. Second harmonic mode in B-mode and fundamental mode for Doppler examinations was used. A stenosis was diagnosed when maximal flow velocity at least doubled in comparison with that of the adjacent segment or when local velocity was at least 2 m/s. Of the left anterior descending coronary artery segments assessed, 34 were proximal, 35 middle, and 34 distal segments. The corresponding figures for circumflex coronary artery segments were 17 proximal and 11 middle segments and for the right coronary artery, 14 proximal and 15 distal segments. No distal circumflex and only 1 mid right coronary artery segment was visualized. Twenty-eight stenoses were diagnosed. Specificity for stenosis detection was 96% to 100% and sensitivity was 62% to 66%. Echo-cardiography was unable to document occlusions. Transthoracic echocardiography allows for coronary artery assessment in a significant portion of patients scheduled for coronary angiography. It may be used to document the presence of coronary artery stenosis. With further technologic improvements, transthoracic echocardiography could enable the monitoring of the restenosis process after percutaneous transluminal coronary angioplasty/stent intervention and coronary artery luminal narrowing after heart transplantation.

Adult↗
PubMed2000

Effect of verapamil on systolic and diastolic coronary blood flow velocity in asymptomatic and mildly symptomatic patients with hypertrophic cardiomyopathy.

OBJECTIVE: To assess non-invasively the effect of verapamil treatment on coronary blood flow velocity in asymptomatic and mildly symptomatic patients with hypertrophic cardiomyopathy. DESIGN: High frequency transthoracic Doppler echocardiography was used to compare resting phasic coronary blood flow velocity before and after a one month period of verapamil treatment in 17 patients (14 men and three women) with non-obstructive hypertrophic cardiomyopathy. Eighteen healthy subjects formed an age and sex matched control group. Systolic and diastolic coronary blood flow velocity was measured in the distal portion of left anterior descending coronary artery using high frequency transthoracic Doppler echocardiography. Blood flow velocity before and after verapamil was compared in the patients with cardiomyopathy and with the results in the control group. RESULTS: Compared with the controls, patients with hypertrophic cardiomyopathy had increased diastolic coronary blood flow velocity (41.8 (8.1) v 59.9 (21.9) cm/s, p < 0.01) and a lower mean systolic coronary blood flow velocity (18.7 (10.8) v -11.2 (27.5) cm/s, p < 0. 01) before verapamil treatment. A backward pattern of systolic flow, manifested by negative values of coronary blood flow velocity, was recorded in eight of the patients, while no negative values were found in the controls. After verapamil treatment the retrograde systolic blood flow was restored to an anterograde pattern in only one patient. The mean value of systolic coronary blood flow velocity did not change significantly and remained lower than the systolic forward flow velocity in the controls (-3.6 (31.8) v 18.7 (10.8) cm/s, p < 0.05). However, diastolic coronary blood flow velocity decreased significantly after verapamil (59.9 (21.9) v 50.7 (19.5) cm/s p < 0.05), reaching a level comparable with that in the controls (50.7 (19.5) v 41.8 (8.1) cm/s, p > 0.05). CONCLUSIONS: In contrast to healthy subjects, in non-obstructive hypertrophic cardiomyopathy the systolic pattern of coronary blood flow was heterogeneous (both retrograde and anterograde), and diastolic coronary blood flow velocity was abnormally increased, despite a lack of significant symptoms. Verapamil treatment did not restore the forward pattern of systolic blood flow but decreased diastolic blood flow velocity to a level comparable with that in healthy subjects.

Adult↗
PubMed2000

[Advanced abdominal angina due to atherosclerosis with atypical celiac arteries].

It is generally accepted that the abdominal angina develops only when at least two of the three splanchnic vessels-mesenteric arteries and the celiac trunk exhibit a critical obstruction. That common opinion does not, however, take into account anatomical variants of arteries supplying the blood to the intestines. We present a case of a wasted, 40 year old male with a wide spread arteriosclerosis and postprandial pain. The ultrasound examination revealed total occlusion of the superior mesenteric artery (SMA). Celiac trunk (CT) and inferior mesenteric artery (IMA) were patent. The ultrasound indicated that only one splanchic vessel was obstructed; the systemic disorder, the neoplasm, as well as the malabsorption were ruled out. An arteriography of the abdominal aorta and of splanchnic arteries confirmed patency of CT and IMA, also lack of flow in the SMA. Atypical origin of the middle colic artery originating from the bed of CT was also shown. Lack of collaterals between IMA and SMA, typically conducting a sufficient blood flow, resulted in a fully symptomatic abdominal angina. Symptoms were relieved following surgical revascularization.

Abdominal Pain↗
PubMed1999

Verapamil improves the response of coronary vasomotion to cold pressor test in asymptomatic and mildly symptomatic patients with hypertrophic cardiomyopathy.

Impaired endothelium-dependent vasodilatation of coronary resistance vessels was previously demonstrated in patients with hypertrophic cardiomyopathy (HC). Therefore, we decided to assess the effect of verapamil administration on the response of diastolic coronary blood flow velocity (CBFV) and the coronary vascular resistance index to the cold pressor test in asymptomatic and mildly symptomatic HC patients. In 10 patients with nonobstructive HC, the CBFV was detected in the distal portion of the left anterior descending coronary artery using high-sensitivity transthoracic Doppler echocardiography. Peak diastolic CBFV, the velocity-time integral of diastolic CBF, and the coronary vascular resistance index (calculated as the mean aortic pressure/CBFV ratio) were measured at baseline and after the cold pressor test. The percentage changes from baseline to the cold pressor test of these parameters were compared before and after 1 month of verapamil therapy. Open-label verapamil changed the decrease in CBFV into an increase in response to the cold pressor test (from -4.1 +/- 6.4% to +11 +/- 10.9%, P < 0.01). A similar reversibility of changes in the velocity-time integral of CBF in response to the cold pressor test after verapamil therapy was observed (from -3.3 +/- 8.3% to +9.6 +/- 10.3%, P < 0.05). Verapamil reversed the response of coronary resistance vessels to the cold pressor test from a +12 +/- 9.8% increase to a -5.2 +/- 10.2% decrease in the coronary vascular resistance index (P < 0.01). We concluded that in asymptomatic and mildly symptomatic HC patients in response to the cold pressor test, treatment with open-label verapamil increased CBF parameters and decreased the coronary vascular resistance index. Verapamil reversed the abnormal vasoconstrictor to vasodilator response of coronary resistance vessels to the cold pressor test. The restoration of the vasodilator response to the cold pressor test by verapamil suggests the potential positive effect of verapamil on endothelium-dependent coronary vasodilation in HC patients. Thus, a randomized blinded trial is now required.

Adult↗
PubMed1999

Impaired response of the forearm resistance but not conductance vessels to reactive hyperemia in hypertrophic cardiomyopathy.

It has been suggested that in hypertrophic cardiomyopathy (HC), vascular abnormalities are not restricted to the heart. Flow-mediated dilation of peripheral conductance arteries (reflecting their endothelial function) has not yet been studied in HC. Our aim was to assess both flow-dependent dilation of the brachial artery and flow responses (dependent on resistance vessels) during forearm reactive hyperemia (RH) in nontreated HC patients. The authors studied 13 HC patients and 14 age- and sex-matched healthy controls. None of them exhibited any factors known to be associated with endothelial dysfunction. Using 7 MHz ultrasound, brachial artery diameter and Doppler flow velocity were measured continuously at baseline and throughout 1 min of RH following 5 min of forearm ischemia induced by inflation of a blood pressure cuff. Arterial diameter and RH flow are expressed as percent changes with respect to the baseline. Flow-dependent dilation was similar in the HC patients and control subjects (7.2 +/- 9.5% vs 9.9 +/- 10.4%, p>0.05). Compared to the control group, RH flow in HC was decreased; however, differences did not reach statistical significance until 60 sec of RH (112 +/- 102% vs 261 +/- 217%, p<0.05; HC vs controls). In HC patients, endothelial function of peripheral conductance arteries is preserved. Hence, a defect in the forearm arterial bed in HC seems to be limited to mechanisms maintaining the dilation of resistance vessels during decreasing RH flow.

Adult↗
PubMed1999

[Balloon angioplasty of branches of the aortic arch].

Balloon angioplasty has become a first-line therapy of symptomatic brachiocephalic occlusive disease. We review our own results of treatment of these lesions for the last two years. 16 patients (18 vessels--6 occlusions) with chronic limb ischaemia (9 cases), vertebrobasilar insufficiency (4 cases), ischemic stroke (2 cases); in one case angioplasty was performed as prevention before major abdominal surgery. Femoral approach was predominantly used; in 3 occlusions brachial approach was chosen. Stents were implanted in 4 cases of poor angioplasty result with severe limb ischaemia. Lesions were crossed in all stenoses and in 4 of 6 occlusions. Residual stenosis < 30% was attained in 10 pts. In 11 cases transstenotic gradient was relieved and a normal flow in vertebral artery was reestablished. There were two cases of acute upper limb ischaemia, one needed surgery. Reversible ulnar nerve paresis was noted in one patient, transient symptoms of postreperfusion syndrome in two. At follow up (mean 12 mo, range 1-30 mo) 1 restenosis was recorded. Balloon angioplasty is easy, safe and effective for treating brachio-cephalic stenoses. Recanalisation of occlusions is more difficult and risky. Treatment of stenoses should not be undully postponed; recanalisation should be reserved for patients with more advanced symptoms of the disease.

Adult↗
PubMed1999

[Coincidence of 20210A prothrombin variant and factor V Leiden predisposing to venous thromboembolism].

Coexistence of inherited and environmental risks leads to the high hazard of venous thromboembolism. In such cases, there might be difficulties in the diagnosis and treatment of recurrent episodes. The importance of Factor V Leiden and prothrombin variant 20210A in the pathogenesis of venous thromboembolic disease, is widely accepted, but the carriership of thrombophilic genes' variants is usually not sufficient for the development of the disease. We report two cases of familial thrombophilia with concurrent presence of prothrombin variant 20210A and factor V Leiden. In a 28-year-old woman: pregnancy, immobilization, obstetric intervention appeared to precipitate the thromboembolic complication. In the second patient, the genetic studies revealed both thrombophilic mutations which could predispose to the recurrent venous thromboembolism, previously thought to be idiopathic. We discuss diagnostic and therapeutic difficulties in such patients.

Adult↗
PubMed1996

Coronary flow reserve and exercise capacity in hypertrophic cardiomyopathy.

The aim of this study was to evaluate the relation of coronary flow velocity (CFV) and coronary flow reserve (CFR) to exercise capacity in ten verapamil-treated patients with hypertrophic cardiomyopathy (HC). Using Doppler transesophageal echocardiography, we assessed diastolic CFV in the proximal left anterior descending coronary artery at baseline and after administering 0.56 mg/kg intravenous dipyridamole. The CFR was calculated as the post-dipyridamole/baseline diastolic CFV ratio. A maximal symptom-limited exercise treadmill test was performed according to a modified Bruce protocol and the exercise capacity was expressed as metabolic equivalents. The mean value for baseline diastolic CFV was 59 +/- 27 cm/s; this increased after dipyridamole to 134 +/- 57 cm/s. The CFR was 2.37 +/- 0.67. Baseline diastolic CFV correlated negatively with both exercise duration (r = -0.69; P < 0.05) and value for metabolic equivalents (r = -0.70; P < 0.05). CFR was weakly and non-significantly related to exercise duration (r = 0.40; P > 0.05) and to the value for metabolic equivalents (r = 0.32; P > 0.05). Shortening of exercise time and decreasing metabolic equivalents were correlated with increased baseline diastolic CFV. Dipyridamole-assessed CFR, was weakly related to parameters of exercise capacity.

Adult↗
PubMed1996

[Familial hyperhomocysteinemia with early development of atherosclerosis].

We describe a large family with hyperhomocysteinemia, the first to be reported in Poland. The proband's coronary complaints appeared at the age of 20, and by the age of 50 he had suffered extensive myocardial infarction. Examination of 17 persons from 4 generations revealed hyperhomocysteinemia in 2 daughters of the proband, while more discrete abnormalities were detected during methionine loading test in two other persons. Levels of cystathionone beta-syntetase and methyleno-FH4 reductase were normal in skin fibroblast culture. Treatment with folic acid and vitamin B12 led to 5-fold depression of plasma homocysteine in the proband, and complete normalization in the other treated member of the family.

Adult↗
PubMed1995

The mechanism of anti-thrombotic, thrombolytic and fibrinolytic actions of camonagrel--a new thromboxane synthase inhibitor.

So far pharmacological consequences of inhibition of thromboxane A2 (TXA2) synthase by imidazole derivatives (e.g., camonagrel or dazoxiben) were linked to suppression of platelet activity. Here we report that in patients with peripheral atherosclerosis or in cats with extracorporeal thrombogenesis treatment with camonagrel is associated with activation of fibrinolysis or thrombolysis. These phenomena seem to be related to the camonagrel-induced shift in metabolism of prostaglandin endoperoxides from TXA2 to prostacyclin (PGI2), although in an in vitro model the involvement of the L-arginine/nitric oxide pathway cannot be excluded. In cats camonagrel (10 mg/kg i.v.) produced not only a fall in TXB2 but also a rise in 6-keto-PGF1 alpha and no change in cyclic-GMP plasma levels. This points to PGI2 rather than to nitric oxide as an in vivo mediator of camonagrel-induced thrombolysis. The crucial role of endogenous PGI2 in the thrombolytic response to camonagrel in cats was evidenced by its blockade following pretreatment of animals with a megadose of aspirin (50 mg/kg i.v.) and lack of any effect on pretreatment with L-NAME (100 micrograms/kg/min, i.v.). Obviously TXA2 synthase inhibitors (e.g., camonagrel) and cyclo-oxygenase inhibitors (e.g., aspirin) antagonize each other in their anti-thrombotic actions and must not be administered at the same time. Furthermore, in patients camonagrel (800 mg orally) suppressed TXA2 generation by 99.5% and doubled the plasma level of 6-keto-PGF1 alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Thrombinogenesis and its pharmacological modulation in atherosclerosis.

Appearance of thrombin in circulating blood can be monitored in the clinical setting by measuring specific thrombin markers, such as fibrinopeptide A, thrombin-antithrombin III or prothrombin fragment 1 + 2. In myocardial infarction monitoring of thrombin activity is of growing clinical interest. High levels of thrombin markers indicate an increased risk to a patient with myocardial infarction. Persistent, high thrombin marker levels, despite heparin anticoagulation, point to ongoing thrombin generation that may necessitate more anticoagulation, increased antiplatelet treatment, angioplasty or, in the future, use of new antithrombotic drugs. Recently, new sensitive methods have been developed to study the reaction of thrombin generation in clotting blood. These methods permitted to demonstrate that, aspirin, contrary to several other antiplatelet drugs, delay the process of thrombin formation. Continuous dampening of thrombin formation by aspirin might be one of the mechanisms responsible for its prophylactic and therapeutic efficacy. Hypercholesterolemic subjects might profit less than others from this type of treatment, since aspirin dampening effects are not so evident in hypercholesterolemia.

Animals↗
PubMed1992

Antiplatelet drugs and generation of thrombin in clotting blood.

Platelets participate in formation of thrombin through secretion of coagulation factors and by providing a catalytic surface on which prothrombinase complex is assembled. We studied the effects of four antiplatelet drugs on thrombin formation in healthy volunteers. Thrombin generation was monitored both in vitro--in recalcified plasma--and ex vivo--in blood emerging from a standardized skin microvasculature injury, which also served to determine bleeding time. A mathematical model has been developed to describe the latter reaction. It is based on estimation of the rate of increase in fibrinopeptide A (FPA), a specific marker of thrombin activity, in blood emerging from skin incisions. Two hours after the ingestion of 500 mg of aspirin, thrombin formation became significantly impaired both in vitro and ex vivo. In contrast, 2 hours after the oral administration of placebo, indomethacin 50 mg, or OKY-046 (a thromboxane synthase inhibitor) 400 mg, thrombinogenesis remained unaltered. Ticlopidine, studied either 3 hours after 500 mg oral administration, or after 5 days of intake at a daily dose of 500 mg, had no effect on thrombin generation. Thus, aspirin, contrary to other antiplatelet drugs, depresses thrombin formation in clotting blood, a phenomenon that might be of clinical relevance. It is suggested that aspirin exerts this effect by acetylating prothrombin and/or macromolecules of platelet membrane.

Adult↗