Coronary flow after stenting.
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Biomedical subjects
Publications and source records attributed to M J Kern.
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A patient with severe medically refractory coronary artery spasm was treated successfully with coronary atherectomy of a mild (40%) left anterior descending artery stenosis. Before the procedure, the patient was dependent on intravenous nitroglycerin because of daily episodes of angina with ST-segment elevation despite receiving multiple combinations of antianginal therapies. Clinical response to coronary atherectomy was prompt and dramatic.
Thirty-four consecutive patients had coronary flow velocity assessed under basal and hyperemic conditions in the proximal and distal coronary artery, followed by rest-stress technetium 99m sestamibi myocardial tomography within 3 months of successful coronary angioplasty. In spite of significant angiographic improvement, 29% of patients had a persistent reversible myocardial perfusion defect associated with a residual abnormality of the proximal-to-distal coronary average peak velocity ratio (p/d APV = 2.2 +/- 1.5 vs 1.1 +/- 0.6; p = 0.02). Patients with an abnormal p/d APV ratio (>1.7) had more numerous angioplasty-zone perfusion defects (4.2 +/- 3.3 vs 0.8 +/- 2.0; p = 0.005). Multivariable analysis of clinical, angiographic, coronary flow, and scintigraphic data demonstrated that the relative risk of cardiac events (n = 11) was greatest in patients with a reversible angioplasty-zone perfusion defect (relative risk, 5.5), poststenotic coronary flow reserve <2.0 (relative risk, 8.3) and p/d APV ratio >1.7 (relative risk, 6.2). Residual basal coronary flow-velocity abnormalities are significant physiologic correlates of stress-induced myocardial perfusion defects and are a prognostic covariable associated with future ischemic cardiac events.
The functional importance and protective nature of the coronary collateral circulation has been well established. There are few data, however, regarding the phasic nature and absolute velocities of collateral flow in patients. The aim of this study was to characterize and quantify ipsilateral coronary collateral blood flow velocity in patients during coronary angioplasty. Coronary collateral flow velocity was measured in 49 patients during coronary angioplasty. Angiographic collateral filling was categorized by the Rentrop grading scale (0 to 3) and by anatomic pathway (epicardial, intramyocardial, or unknown [acutely recruited]). Collateral blood flow velocity was measured with a Doppler-tipped guide wire placed distal to the balloon occlusion in the collateralized vessel. Collateral flow velocity was characterized as predominantly systolic or diastolic, and phasic flow patterns were defined as biphasic (both systolic and diastolic), monophasic (only systolic or diastolic), or bidirectional (antegrade and retrograde velocity). Twenty-three (47%) patients had biphasic flow; 17 (35%) patients had monophasic flow; and 9 (18%) patients had bidirectional flow. Thirty-six (73%) of 49 patients had predominantly systolic flow signals. Epicardial collateral pathways had the highest total flow velocity integral, at 15.0 +/- 7.0 (vs intramyocardial [8.4 +/- 5.7] and acutely recruitable [5.4 +/- 2.1]; p < 0.05). There were no differences in flow velocity integrals among the Rentrop angiographic grades of collateral filling. These data establish three patterns of coronary collateral blood flow and demonstrate that the majority of collateral flow in the ipsllateral receiving vessel occurs during systole. The measurement of coronary collateral flow velocity provides a unique means to study the effects of pharmacologic or mechanical interventions on human collateral blood flow.
The purpose of this study was to examine the influence of sequential percutaneous transluminal coronary rotational atherectomy (PTCRA) and coronary angioplasty on coronary blood flow reserve in patients. Rotational coronary atherectomy restores lumen patency by partially ablating fibrocalcific plaque, releasing microparticulate debris into the distal coronary circulation. Adjunctive balloon angioplasty is usually performed to optimize the angiographic luminal dimensions. Serial alterations in coronary physiology have not been reported. Fourteen lesions in 13 patients were treated by sequential rotational atherectomy followed by adjunctive balloon angioplasty. Poststenotic baseline coronary blood flow velocity was measured by using a Doppler flow wire (FloWire, Cardiometrics, Inc., Mountain View, Calif.), and coronary blood flow was calculated by using the distal vessel cross-sectional area obtained by quantitative coronary angiography. Data were acquired at baseline and during hyperemia (12 to 18 microg of intracoronary adenosine), before and after PTCRA, and again after balloon angioplasty. The mean stenosis decreased from 76 percent +/- 12 percent at baseline to 21 percent +/- 11 percent at the completion of the procedure (p<0.01). The minimal luminal diameter (by quantitative coronary angiography) was 0.7 +/- 0.4 mm at baseline, increased to 1.9 +/- 0.4 mm after rotational atherectomy (p<0.01), and increased to 2.4 +/- 0.5 mm after balloon angioplasty (p<0.01 versus baseline and PTCRA). Distal (poststenotic) coronary blood flow at baseline was 47 +/- 23 ml/min and 57 +/- 38 ml/min during hyperemia. After PTCRA, coronary blood flow increased to 104 +/- 59 ml/min and to 132 +/- 73 ml/min with hyperemia. After adjunctive angioplasty, coronary blood flow was 84 +/- 40 ml/min (p=not significant [NS] vs PTCRA) and increased to 143 +/- 81 ml/min with hyperemia (p=NS vs PTCRA). The poststenotic coronary flow reserve increased from an initial value of 1.1 +/- 0.2 ml/min to 1.3 +/- 0.3 ml/min after PTCRA (p=NS vs baseline) and to 1.6 +/- 0.3 ml/min after adjunctive balloon angioplasty (p<0.01 vs p=NS vs PTCRA). PTCRA significantly increased resting coronary blood flow. Adjunctive balloon angioplasty did not significantly augment resting or hyperemic coronary blood flow more than that achieved by rotational atherectomy alone. These data demonstrate that PTCRA alone improves baseline coronary blood flow with minimal additional physiologic change after adjunctive balloon angioplasty.
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Integration of coronary blood flow velocity measurements into interventional procedures has enhanced our understanding of coronary flow dynamics. The coronary physiology of rotational atherectomy, with and without adjunctive coronary angioplasty, has not been well-defined. This review describes the coronary physiology induced by rotational atherectomy. Serial coronary blood flow and translesional hemodynamics, measured following rotational atherectomy and again after adjunctive balloon angioplasty, indicate that coronary blood flow and flow reserve may not be normalized despite significant angiographic improvements after rotational atherectomy alone and after adjunctive balloon angioplasty.
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BACKGROUND: Intravascular ultrasound imaging detects epicardial intimal thickening in the majority of heart transplant recipients with angiographically normal epicardial coronary arteries. Although coronary artery vasoreactivity is abnormal after cardiac transplantation, intimal thickening does not appear to affect conduit vessel responses. However, the effect of intimal thickening on both conduit and resistance vessel responses, as measured by changes in volumetric coronary blood flow (CBF), is unknown. METHODS AND RESULTS: Epicardial coronary artery conductance and microvascular resistance vessel responses were studied after intracoronary adenosine and nitroglycerin administration in 36 orthotopic heart transplant recipients 1 month to 7 years after transplantation. Sequentially measured coronary flow average peak velocity ([APV, cm/s] 0.018 in Doppler guide wire) and epicardial luminal cross-sectional area ([CSA, mm2] 4.3F 30-MHz ultrasound catheter) data were obtained at baseline and during peak hyperemia after administration of 12 to 18 micrograms IC adenosine and 150 to 200 micrograms IC nitroglycerin. Volumetric CBF (mL/min) was calculated as CBF = APV (cm/s) x CSA (mm2) x 60 seconds/1 min x 1 cm2/100 mm2 x 0.5. Measurements were made from a discrete position in the proximal left anterior descending (LAD) artery (n = 22), mid-LAD artery (n = 7), proximal circumflex artery (n = 6), and proximal right coronary artery (n = 1). Intimal thickening was present in 19 of 32 patients (60%). Both adenosine and nitroglycerin increased APV (from 18.9 +/- 4.9 to 56.0 +/- 11.5 cm/s for adenosine and from 20.2 +/- 5.3 to 49.1 +/- 11.5 cm/s for nitroglycerin; both P < .05). Coronary flow velocity reserve was significantly higher for adenosine compared with nitroglycerin (3.1 +/- 0.6 versus 2.5 +/- 0.7, respectively; P < .001). Epicardial luminal CSA was unchanged during adenosine hyperemia compared with baseline (17.4 +/- 3.8 versus 17.3 +/- 4.0 mm2, respectively; P = NS) but was significantly greater during nitroglycerin hyperemia compared with baseline (18.7 +/- 3.8 versus 17.3 +/- 4.0 mm2, 6.2 +/- 3.6% change; P < .05). Baseline CBF was similar before drug administration. Hyperemic adenosine and nitroglycerin CBF responses (297 +/- 99 and 276 +/- 87 mL/min, respectively; P = NS) and CBF reserve (3.0 +/- 0.7 and 2.7 +/- 0.7, respectively; P = NS) were not significantly different. Importantly, intimal thickening did not diminish resting or hyperemic APV, coronary flow velocity reserve, luminal CSA, CBF, or CBF reserve responses. CONCLUSIONS: In this study of angiographically normal heart transplant recipients, epicardial intimal thickening does not diminish conduit and resistance vessel responses during endothelial-independent vasodilator administration.
BACKGROUND: There are few data comparing clinical outcome and potential indications for routine post-myocardial infarction cardiac catheterization and revascularization of patients who sustain a non-Q-wave versus Q-wave infarct after thrombolytic therapy. METHODS AND RESULTS: A secondary analysis of 2634 patients enrolled in the TIMI II trial with a first myocardial infarction was performed to determine 6-week and 1-year cardiac event rates and identify clinical and angiographic differences between the 1867 patients (70.9%) who evolved a Q-wave infarct and the 767 patients (29.1%) who sustained a non-Q-wave infarct after treatment with intravenous thrombolytic therapy. Male sex (85.3% versus 75.6%; P < .001) and anterior wall infarcts (53.8% versus 43.7%; P < .001) were more frequent in the Q-wave versus the non-Q-wave group. During recombinant tissue-type plasminogen activator (rTPA) infusion, a greater percentage of non-Q-wave patients (37.3% versus 23.5%; P = .001) had normalization of initial ST-segment elevation. Infarct-related artery patency (TIMI flow grade 2 or 3) (P = .02), complete infarct-related artery reperfusion (TIMI 3 flow grade) (P < .001), and the percentage of patients with a predischarge resting left ventricular ejection fraction > 55% (P < .001) were greater in the non-Q-wave group. New congestive heart failure during hospitalization developed more frequently in Q-wave patients (18.9% versus 11.6%; P < .001). After 42 days, the occurrences of reinfarction (P = .76), death (P = .76), and combined death or reinfarction (P = .43) were similar in patients assigned to the invasive or conservative postlytic management strategy, regardless of infarct type. One-year mortality was 3.4% versus 4.4% for non-Q-wave versus Q-wave infarct type, respectively (P = .25). CONCLUSIONS: Angiographic and clinical differences were observed between patients who present with initial ST-segment elevation and evolve early non-Q-wave versus Q-wave myocardial infarcts after treatment with rTPA, heparin, and aspirin. Early mortality and adverse clinical cardiac events in these patients are not significantly different after a conservative compared with an invasive treatment strategy, regardless of whether the infarct type is non-Q wave or Q wave.
Although quantitative coronary angiography (QCA) has been used to determine lesion severity, angiographically derived parameters of translesional physiology have not been compared with those directly measured in the same patients. Thus, the aim of this study was to correlate QCA-derived translesional pressure and flow data with directly measured data in patients. QCA (DCI-ACA program), translesional pressure gradient (2.2Fr fluid-filled tracking catheter), and intracoronary Doppler flow velocity (0.018-inch FloWire) measurements were simultaneously performed in 28 arteries (25 patients). Mean diameter stenosis was 51 +/- 2.3% (range 29 to 73). No patient had left ventricular hypertrophy or valvular heart disease. The arteries studied were left anterior descending in 14, circumflex in 8, and right coronary in 6 patients. Stenotic flow reserve and baseline and maximal gradients were calculated by the DCI program. Coronary flow reserve and baseline and maximal hyperemic gradients were also directly measured distal to the stenosis after administration of intracoronary adenosine (12 to 18 micrograms). QCA-derived pressure gradients did not correlate with the measured gradients at baseline (r2 = 0.005; p = 0.73) or at maximal hyperemia (r2 = 0.1; p = 0.13). No correlation was found between the QCA-predicted flow reserve and the coronary flow reserve measured distal to the stenosis (r2 = 0.02; p = 0.46). Furthermore, stenotic flow reserve and measured gradient were not significantly correlated (r2 = 0.1; p = 0.16). In this range of stenoses of intermediate severity, there was no correlation between the measured pressure gradient or coronary flow reserve and lesion diameter or cross-sectional area by QCA.(ABSTRACT TRUNCATED AT 400 WORDS)
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During normal flow velocity recording, various physiologic or technical problems may appear which can produce confusing flow signals. This section of Interventional Physiology reviews the patterns of normal coronary flow velocity and examines several artifacts and other features encountered in clinical practice. Recognition of these variations will help the interventional cardiologist to differentiate between physiologic and pathologic events.
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The unique observations of contralateral and ipsilateral coronary artery collateral supply before and after angioplasty suggest highly responsive conduits to hemodynamic conditions. The study of collateral supply system is not only significant for our current understanding of the dynamic behavior of the collateral circulation, but may also have important clinical implications for the treatment of patients with a chronic coronary occlusion.