Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the presence, mechanism, and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 50 patients underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared to patients without hypertrophic cardiomyopathy, their basal coronary flow, myocardial oxygen consumption, and left ventricular end-diastolic pressure were significantly higher. Further, the 23 patients with basal obstruction to left ventricular outflow had a significantly higher basal great cardiac vein flow and oxygen consumption than the 27 patients without basal obstruction. During pacing to heart rates of 100 and 130 bpm (the anginal threshold for 41 of 50 patients), those with basal obstruction still demonstrated significantly higher coronary flow and oxygen consumption. Most patients, regardless of the presence or absence of obstruction, had metabolic evidence of ischemia, often severe. At a heart rate of 150, most patients with basal obstruction demonstrated an actual decline in coronary flow, which correlated with an increase in left ventricular filling pressures and more severe metabolic evidence of ischemia. In those without obstruction, ischemia occurred at a lower coronary flow, suggesting more impaired coronary flow delivery than those with obstruction. Abnormalities in oxygen extraction were noted in both groups. Thus, obstruction to left ventricular outflow results in higher basal and stress-induced coronary flow and oxygen requirements, related to elevated left ventricular systolic pressures, resulting in rapid exhaustion of coronary flow reserve during stress. Patients without obstruction, with lower left ventricular systolic pressures, may have greater impairment of flow delivery during stress as a cause of myocardial ischemia.
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PMID:Myocardial ischemia in hypertrophic cardiomyopathy. 343 62

Many patients with hypertrophic cardiomyopathy (HCM) have signs and symptoms or metabolic and hemodynamic evidence of myocardial ischemia and dysfunction in the absence of extramural coronary atherosclerosis. To investigate the possibility that a form of "small vessel disease" could account for these findings, a histologic analysis of left ventricular myocardium obtained at necropsy was carried out in 48 patients with hypertophic cardiomyopathy and in 68 controls with either normal hearts or acquired heart disease. In HCM, abnormal intramural coronary arteries (IMCA) were characterized by thickening of the vessel wall and an apparent decrease in luminal size (external arterial diameter less than 1500 micron; average 300 micron). The wall thickening was due to proliferation of medial and/or intimal components, particularly smooth muscle cells and collagen. Of the 48 patients with HCM,40 (83%) had abnormal IMCAs located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (nine patients); an average of 3.0 +/- 0.7 IMCA were identified per tissue section. Altered IMCAs were also significantly more common in tissue sections having considerable myocardial fibrosis (31 out of 42, 74%) than in those with no or mild fibrosis (31 or 102, 30%; p less than 0.001). Abnormal IMCA wera also identified in 3 out of 8 infants who died of HCM before 1 year of age. In contrast, only rare altered IMCA were identified in six (9%) of the 69 control patients, and those arteries showed only mild thickening of the wall and minimal luminal narrowing (abnormal IMCA per section: 0.1 +/- 0.05: p less than 0.001). Moreover, of those patients who did show abnormal IMCA, such vessels were about twenty times more frequent in patients with HCM (0.9 +/- 0.2/cm2 myocardium) than in controls (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal IMCA with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with HCM at necropsy, and may represent a congenital component of the underlying cardiomyopathic process. Although the clinical significance of "small vessel coronary artery disease" in HCM is unclear, the occurrence of structurally altered IMCA within or adjacent to areas of substantial myocardial fibrosis suggests a causal role for these arteries in producing ischemia.
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PMID:Morphologic evidence for "small vessel disease" in patients with hypertrophic cardiomyopathy. 343 79

Myocardial ischemia may play a critical role in the symptomatic presentation and natural history of hypertrophic cardiomyopathy (HCM). To assess the relative prevalence and functional significance of myocardial perfusion abnormalities in patients comprising the broad clinical spectrum of HCM, we studied 72 patients (ages 12 to 69 years, mean 40) using thallium-201 emission computed tomography. Imaging was performed immediately after maximal exercise and again after a 3 hr delay. Regional perfusion defects were identified in 41 of the 72 patients (57%). Fixed or only partially reversible defects were evident in 17 patients, 14 of whom (82%) had left ventricular ejection fractions of less than 50% at rest. Twenty-four patients demonstrated perfusion defects during exercise that completely reversed at rest; all had normal or hyperdynamic left ventricular systolic function (ejection fraction greater than or equal to 50%). Perfusion abnormalities were present in all regions of the left ventricle. However, the fixed defects were observed predominantly in segments of the left ventricular wall that were of normal or only mildly increased (15 to 20 mm) thickness; in contrast, a substantial proportion (41%) of the completely reversible defects occurred in areas of moderate-to-marked wall thickness (greater than or equal to 20 mm, p less than .001). Neither a history of chest pain nor its provocation with treadmill exercise was predictive of an abnormal thallium study, since regional perfusion defects were present in 10 of 18 (56%) completely asymptomatic patients, compared with 31 of 54 (58%) symptomatic patients. These data indicate that myocardial perfusion abnormalities occur commonly among patients with HCM. Fixed or only partially reversible defects suggestive of myocardial scar and/or severe ischemia occur primarily in patients with impaired systolic performance. Completely reversible perfusion abnormalities occur predominantly in patients with normal or supranormal left ventricular systolic function. Such dynamic changes in regional thallium activity may reflect an ischemic process that contributes importantly to the clinical manifestations and natural history of HCM.
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PMID:Myocardial perfusion abnormalities in patients with hypertrophic cardiomyopathy: assessment with thallium-201 emission computed tomography. 349 97

Fifty patients with hypertrophic cardiomyopathy underwent invasive study of coronary and myocardial hemodynamics in the basal state and during the stress of pacing. The 23 patients with basal obstruction (average left ventricular outflow gradient, 77 +/- 33 mm Hg; left ventricular systolic pressure, 196 +/- 33 mm Hg, mean +/- 1 SD) had significantly lower coronary resistance (0.85 +/- 0.18 versus 1.32 +/- 0.44 mm Hg X min/ml, p less than 0.001) and higher basal coronary flow (106 +/- 20 versus 80 +/- 25 ml/min, p less than 0.001) in the anterior left ventricle, associated with higher regional myocardial oxygen consumption (12.4 +/- 3.6 versus 8.9 +/- 3.3 ml oxygen/min, p less than 0.001) compared with the 27 patients without obstruction (mean left ventricular systolic pressure 134 +/- 18 mm Hg, p less than 0.001). Myocardial oxygen consumption and coronary blood flow were also significantly higher at paced heart rates of 100 and 130 beats/min (the anginal threshold for 41 of the 50 patients) in patients with obstruction compared with those without. In patients with obstruction, transmural coronary flow reserve was exhausted at a heart rate of 130 beats/min; higher heart rates resulted in more severe metabolic evidence of ischemia with all patients experiencing chest pain, associated with an actual increase in coronary resistance. Patients without obstruction also demonstrated evidence of ischemia at heart rates of 130 and 150 beats/min, with 25 of 27 patients experiencing chest pain. In this group, myocardial ischemia occurred at significantly lower coronary flow, higher coronary resistance and lower myocardial oxygen consumption, suggesting more severely impaired flow delivery in this group compared with those with obstruction. Abnormalities in myocardial oxygen extraction and marked elevation in filling pressures during stress were noted in both groups. Thus, obstruction to left ventricular outflow is associated with high left ventricular systolic pressure and oxygen consumption and therefore has important pathogenetic importance to the precipitation of ischemia in patients with hypertrophic cardiomyopathy. Patients without obstruction may have greater impairment in coronary flow delivery during stress.
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PMID:Differences in coronary flow and myocardial metabolism at rest and during pacing between patients with obstructive and patients with nonobstructive hypertrophic cardiomyopathy. 359 95

The case reported herein illustrates an unusual form of nonobstructive hypertrophic cardiomyopathy which was associated with Wolff-Parkinson-White syndrome, myocardial ischemia and necrosis despite normal coronary arteries. The patient is unique since the hypertrophied myocardial segment was localized exclusively to the posterolateral free wall. Quantitative thallium-201 scintigraphy demonstrated reversible ischemia that corresponded precisely with this region of posterolateral hypertrophy. While the exact mechanism for ischemia in patients with hypertrophic cardiomyopathy and normal coronary arteries remains controversial, a functional rather than anatomic disturbance of blood flow seems likely.
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PMID:Hypertrophic cardiomyopathy and myocardial ischemia with normal coronary arteries. 360 9

To determine the prevalence and significance of the systolic compression of the anterior descending coronary artery in hypertrophic cardiomyopathy, we studied 54 consecutive patients out of a catheterization laboratory population of 1619. This angiographic finding was found to be more prevalent (P less than 0.001) and severe in myopathic than in secondary hypertrophy. Complete systolic occlusion occurred in 5 of the 6 patients with nonobstructive cardiomyopathy showing the systolic narrowing. Severe septal squeezing was also present in these cases and the diastolic time lag to refill the distal branches reached 20-33% of the diastolic period. This subset of patients showed the least dynamic anterior wall contraction (P less than 0.001) and the highest incidence of thallium-201 perfusion defects (P less than 0.05) and of recurrent cardiac arrest (P less than 0.05). We conclude that severe systolic compression of the descending coronary artery in hypertrophic cardiomyopathy may be an angiographic marker of the myopathic hypertrophy extending to the anterior wall and might contribute to ischemia when the time to restore the distal perfusion is greatly delayed.
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PMID:Systolic compression of coronary artery in hypertrophic cardiomyopathy. 375 68

Abnormal left ventricular (LV) diastolic performance is a characteristic feature of hypertrophic cardiomyopathy (HC) and an important contributor to the development of symptoms. Impaired diastolic filling of the hypertrophied left ventricle results from both diminished distensibility and prolonged or incomplete relaxation. LV distensibility is not only influenced by fixed anatomic abnormalities (such as fibrosis or hypertrophy) that determine the passive elastic properties of the left ventricle, but also is modulated by the dynamics of myocardial relaxation: prolonged or incomplete LV relaxation may restrict the rate and extent of LV filling and result in altered pressure-volume relations throughout diastole. Several studies indicate that impaired LV relaxation and filling in HC may be modified favorably by verapamil or nifedipine administered on a short-term basis in the catheterization laboratory, associated with improved diastolic pressure-volume relations. Verapamil also improves LV filling during oral therapy. Improved indexes of LV filling correlate with symptomatic improvement, both short-term and long-term: Approximately 80% of patients having a persistent increase in peak LV filling rate have persistent improvement in objective exercise tolerance compared with preverapamil values. Altered LV relaxation and filling are also often observed in patients with coronary artery disease (CAD) after myocardial infarction or during acute ischemia. Moreover, impaired filling occurs under resting conditions in many patients who have normal systolic function and no evidence of previous infarction. Nifedipine improves indexes of LV relaxation and distensibility during pacing-induced ischemia and verapamil improves indexes of LV filling at rest and during exercise-induced ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of calcium-channel blocking agents on left ventricular diastolic function in hypertrophic cardiomyopathy and in coronary artery disease. 388 11

To study the mechanism and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 20 patients (nine with resting left ventricular outflow tract obstruction greater than or equal to 30 mm Hg) with a history of angina pectoris and angiographically normal coronary arteries underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared with 28 control subjects without hypertrophic cardiomyopathy, their resting coronary blood flow was higher (91 +/- 27 vs 66 +/- 17 ml/min; p less than .001) and their coronary resistance was lower (1.13 +/- 0.38 vs 1.55 +/- 0.45 mm Hg/ml/min; p less than .001). Left ventricular end-diastolic pressure (16 +/- 6 vs 11 +/- 3 mm Hg; p less than .001) and pulmonary arterial wedge pressure (13 +/- 5 vs 7 +/- 3 mm Hg; p less than .001) were significantly higher in patients with hypertrophic cardiomyopathy. During pacing, coronary flow rose in both groups, although coronary and myocardial hemodynamics differed greatly. In contrast to the linear increase in flow in control subjects up to heart rate of 150 beats/min (66 +/- 17 to 125 +/- 28 ml/min), patients with hypertrophic cardiomyopathy demonstrated an initial rise in flow to 133 +/- 31 ml/min at an intermediate heart rate of 130 beats/min. At this point, 12 of 20 patients developed their typical chest pain. With continued pacing to a heart rate of 150 beats/min, mean coronary flow fell to 114 +/- 29 ml/min (p less than .002), with 18 of 20 patients experiencing their typical chest pain and metabolic evidence of myocardial ischemia. This fall in coronary flow was associated with a substantial rise in left ventricular end-diastolic pressure (30 +/- 9 mm Hg immediately after peak pacing). In the 14 patients whose coronary flow actually fell from intermediate to peak pacing, the rise in left ventricular end-diastolic pressure in the same interval was greater than that of the six patients whose flow remained unchanged or increased (11 +/- 8 vs 2 +/- 2 mm Hg; p less than .01). In addition, despite metabolic and hemodynamic evidence of myocardial ischemia, the arteriovenous O2 difference actually narrowed at peak pacing. Thus most patients with hypertrophic cardiomyopathy achieved maximum coronary vasodilation and flow at modest increases in heart rate. Elevation in left ventricular filling pressure, probably related to ischemia-induced changes in ventricular compliance, was associated with a decline in coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures. 403 83

We describe a case of myocardial bridging of the anterior descending coronary artery associated with a non-obstructive hypertrophic cardiomyopathy which was corrected by surgery because of a poor response to standard drug therapy. The clinical significance of the association is discussed. The possibility of repair by surgery should be considered when an area of ischemia supplied by the affected vessel is detected and previous medical treatment has been ineffective.
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PMID:Myocardial bridging and hypertrophic cardiomyopathy: relief of ischemia by surgery. 404 May 1

Diltiazem, nifedipine, and verapamil inhibit calcium entry into cells via different mechanisms with different pharmacologies. They display different relative effects on different cardiovascular functions, a complex interplay of direct actions and adrenergic reflexes. Peripheral arterial vasorelaxation causes adrenergic reflex activity which opposes their direct negative chronotropic, dromotropic, inotropic, and hypotensive actions. Verapamil's most potent activity is electrophysiologic, and nifedipine's effects are hemodynamic; diltiazem acts like a less-potent combination of verapamil and nifedipine. All three drugs are efficacious in angina. These three drugs may not be interchangeable in all patients, but individualization of therapy is possible. Future indications for calcium channel blocker therapy may include hypertrophic cardiomyopathy, cerebral vasospasm, migraine headaches, pulmonary hypertension, asthma, esophageal spasm, intestinal ischemia, Raynaud's phenomenon, dysmenorrhea, and premature labor.
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PMID:Calcium channel blockers in emergency medicine. 638 Mar 52


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