Marek Krzanowski

Imaging of all three coronary arteries by transthoracic echocardiography. an illustrated guide

BackgroundImprovements in ultrasound technology has enabled direct, transthoracic visualization of long portions of coronary arteries : the left anterior descending (LAD), circumflex (Cx) and right coronary artery (RCA). Transthoracic measurements of coronary flow velocity were proved to be highly reproducible and correlated with invasive measurements. While clinical applications of transthoracic echocardiography (TTE) of principal coronary arteries are still very limited they will likely grow. The echocardiographers may therefore be interested to know the ultrasonic views, technique of examination and be aware where to look for coronary arteries and how to optimize the images.MethodsA step-by-step approach to direct, transthoracic visualization of the LAD, Cx and RCA is presented. The technique of examination is discussed, correlations with basic coronary angiography views and heart anatomy are shown and extensively illustrated with photographs and movie-pictures. Hints concerning optimization of ultrasound images are presented and artifacts of imaging are discussed.ConclusionsDirect, transthoracic examination of the LAD, Cx and RCA in adults is possible and may become a useful adjunct to other methods of coronary artery examination but studies are needed to establish its role.

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.

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

Summary. 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 by verapamil cold pressor test suggests the potential positive effect of verapamil on endothelium-dependent coronary vasodilatation in HC patients. Thus, a randomized blinded trial is now required.

Coronary flow reserve and exercise capacity in hypertrophic cardiomyopathy

SummaryThe 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 postdipyridamole/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 ± 27cm/s; this increased after dipyridamole to 134 ± 57cm/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.

Reduced coronary flow reserve in Anderson-Fabry disease measured by transthoracic Doppler echocardiography.

Coronary flow reserve was assessed in a patient with Anderson-Fabry disease complicated by symmetric left ventricular hypertrophy. Coronary flow reserve was measurable in all three major coronary arteries providing an opportunity to compare regional coronary flow reserve from different vascular beds. In this patient all the three vascular beds supplied diffusely hypertrophied myocardium. Coronary flow disturbances in small intramyocardial perforating arteries were visible. The coronary flow reserve was reduced to a similar level (around to 2.0) in all three major arteries. In our patient with Anderson-Fabry disease, the coronary vasodilatation was blunted in a diffuse pattern corresponding to the myocardial hypertrophy distribution. In small intramyocardial arteries coronary flow was also disturbed. Accordingly, retrograde systolic flow and accelerated anterograde diastolic flow were documented.

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 abnormali ties 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 dysfunc tion. 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.

Verapamil improves the pacing-induced vasodilatation in symptomatic patients with hypertrophic cardiomyopathy

The purpose of the study was to assess the effect of verapamil on the response of diastolic coronary flow velocity and coronary vascular resistance to pacing in symptomatic patients with hypertrophic cardiomyopathy. In 14 patients with hypertrophic cardiomyopathy, the coronary flow velocity was detected in the left anterior descending coronary artery using transthoracic Doppler echocardiography. The peak diastolic coronary flow velocity and coronary vascular resistance was measured at baseline and during pacing. Changes of these parameters induced by the pacing (expressed as the percentage of baseline values) were compared on verapamil treatment and after verapamil withdrawal. The same measurements were obtained in ten control subjects. The results show that, in hypertrophic cardiomyopathy patients, increase in coronary flow velocity during pacing was significantly higher on than off verapamil therapy (64.8+/-32.5 vs. 41.1+/-21.3%, P<0.05). In control subjects, pacing-induced increase in coronary flow velocity was comparable to changes in coronary flow velocity in hypertrophic cardiomyopathy patients receiving verapamil (80.2+/-18.4 vs. 64.8+/-32.5%, P>0.05). After verapamil withdrawal in hypertrophic cardiomyopathy patients, coronary flow velocity increase during pacing was significantly lower than in control subjects (41.1+/-21.3 vs. 80.2+/-18.4%, P<0.05). During pacing the coronary vascular resistance decreased more on verapamil than after drug withdrawal (-34.7+/-11.7 vs. -24.6+/-12.9%, P<0.05). In control subjects the coronary vascular resistance decreased during pacing -38.6+/-6.3% to similar extent as in hypertrophic cardiomyopathy patients on verapamil. We can conclude that endothelium-dependent vasodilatation during pacing was impaired in symptomatic patients with hypertrophic cardiomyopathy. Verapamil treatment was able to restore adequate vasodilator response to pacing stress.

The Effect of Verapamil on Response of Coronary Vasomotion to Handgrip Exercise in Symptomatic Patients with Hypertrophic Cardiomyopathy

AbstractObjectives. 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.

Percutaneous Transluminal Angioplasty in Patients with Peripheral Arterial Disease Does Not Affect Circulating Monocyte Subpopulations

Monocytes are mononuclear cells characterized by distinct morphology and expression of CD14 and CD16 surface receptors. Classical, quiescent monocytes are positive for CD14 (lipopolysaccharide receptor) but do not express Fc gamma receptor III (CD16). Intermediate monocytes coexpress CD16 and CD14. Nonclassical monocytes with low expression of CD14 represent mature macrophage-like monocytes. Monocyte behavior in peripheral arterial disease (PAD) and during vessel wall directed treatment is not well defined. This observation study aimed at monitoring of acute changes in monocyte subpopulations during percutaneous transluminal angioplasty (PTA) in PAD patients. Patients with Rutherford 3 and 4 PAD with no signs of inflammatory process underwent PTA of iliac, femoral, or popliteal segments. Flow cytometry for CD14, CD16, HLA-DR, CD11b, CD11c, and CD45RA antigens allowed characterization of monocyte subpopulations in blood sampled before and after PTA (direct angioplasty catheter sampling). Patients were clinically followed up for 12 months. All 61 enrolled patients completed 12-month follow-up. Target vessel failure occurred in 12 patients. While absolute counts of monocyte were significantly lower after PTA, only subtle monocyte activation after PTA (CD45RA and β-integrins) occurred. None of the monocyte parameters correlated with long-term adverse clinical outcome. Changes in absolute monocyte counts and subtle changes towards an activation phenotype after PTA may reflect local cell adhesion phenomenon in patients with Rutherford 3 or 4 peripheral arterial disease.

Involvement of CD8+ T cell subsets in early response to vascular injury in patients with peripheral artery disease in vivo

AIMS Adaptive immunity is critical in vascular remodelling following arterial injury. We hypothesized that acute changes in T cells at a percutaneous transluminal angioplasty (PTA) site could serve as an index of their potential interaction with the injured vascular wall. METHODS AND RESULTS T cell subsets were characterised in 45 patients with Rutherford 3-4 peripheral artery disease (PAD) undergoing PTA. Direct angioplasty catheter blood sampling was performed before and immediately after the procedure. PTA was associated with an acute reduction of α/β-TcR CD8+ T cells. Further characterisation revealed significant reduction in pro-atherosclerotic CD28nullCD57+ T cells, effector (CD45RA+CCR7-) and effector memory (CD45RA-CCR7-) cells, in addition to cells bearing activation (CD69, CD38) and tissue homing/adhesion markers (CD38, CCR5). CONCLUSIONS The acute reduction observed here is likely due to the adhesion of cells to the injured vascular wall, suggesting that immunosenescent, activated effector CD8+ cells have a role in the early vascular injury immune response following PTA in PAD patients.