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Resolution of angina pectoris and improvement of the coronary flow reserve after ranolazine treatment in a woman with isolated impaired coronary microcirculation.

Santoro A, Schiano Lomoriello V, Santoro C, Muscariello R, Galderisi M - Case Rep Cardiol (2013)

Bottom Line: The improvement of both symptoms and coronary microvascular function is strictly linked to the mechanism of action of the drug.Ranolazine induces in fact a reduction of the intracellular late sodium current that leads to a reduction of the intracellular calcium concentration thus producing a better myocardial diastolic relaxation process which in its turns enhances the myocardial perfusion.The ranolazine acts therefore as a lusitropic drug that improves the diastolic dysfunction and the segmental ischemia thus affecting one of the first steps of the ischemic cascade.

View Article: PubMed Central - PubMed

Affiliation: Cardioangiology with CCU, Department of Clinical and Experimental Medicine, Federico II University Hospital, 80131 Naples, Italy.

ABSTRACT
In a 61-year-old woman with well controlled arterial hypertension, hypercholesterolemia, and smoke and suffering from recurrent angina pectoris despite angiographically normal epicardial coronary vessels and maximal therapy, the replacement of nitrates with novel antiangina drug ranolazine, after 6-month therapy, induced a complete relief of angina and a relevant rising of the transthoracic Doppler-derived coronary flow reserve (CFR). The present clinical case underlines therefore how in patients with chronic ischemic heart disease without epicardial coronary stenosis ranolazine can induce an improvement till the complete solution of the angina symptoms and a substantial increase of CFR as expression of the enhancement of the microvascular coronary function. The improvement of both symptoms and coronary microvascular function is strictly linked to the mechanism of action of the drug. Ranolazine induces in fact a reduction of the intracellular late sodium current that leads to a reduction of the intracellular calcium concentration thus producing a better myocardial diastolic relaxation process which in its turns enhances the myocardial perfusion. The ranolazine acts therefore as a lusitropic drug that improves the diastolic dysfunction and the segmental ischemia thus affecting one of the first steps of the ischemic cascade.

No MeSH data available.


Related in: MedlinePlus

Mechanism of action of ranolazine. The pharmacologically induced reduction of the late sodium current ameliorates the myocardial diastolic relaxation by reducing the diastolic wall stress. This finally produces an improvement of segmental myocardial ischemia.
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fig6: Mechanism of action of ranolazine. The pharmacologically induced reduction of the late sodium current ameliorates the myocardial diastolic relaxation by reducing the diastolic wall stress. This finally produces an improvement of segmental myocardial ischemia.

Mentions: According to the recommendation of the European Association of Echocardiography [6], the stress echo with dipyridamole represents a very accurate test in order to distinguish an epicardial coronary stenosis from an isolated coronary microvascular dysfunction: the first one shows a reduction of the CFR with impairment of the regional wall motion and the latter shows a reduction of the CFR without regional wall motion abnormalities or even a supernormal wall motion. In our experience a reduced CFR + normal regional wall motion pointed out an impaired function of the coronary microcirculation, where a previous coronary angiography had already shown a coronary three free of stenosis. In this setting, after almost 6 months of therapy, ranolazine caused a relevant rising of the CFR that is strictly linked to its mechanism of action. Ranolazine induces a reduction of the intracellular late sodium current that leads to a reduction of the intracellular calcium concentration thus producing a diastolic relaxation improvement which in its turns enhances the myocardial perfusion [8]. The coronary flow is substantially greater during the diastolic phase of the cardiac cycle thus it is evident that the smaller vessels, the ones that make up the microvascular circulation, are the one that benefit more from the effect of the decompression caused by ranolazine during the myocardial relaxation process. The ranolazine acts therefore as a lusitropic drug that improves the diastolic dysfunction and the segmental ischemia thus affecting one of the first steps of the ischemic cascade (Figure 6). The results of the presented clinical case reflect the ones produced by a recently published clinical study where a 4-week therapy with ranolazine showed to be useful reducing the recurrence of the angina symptoms and improving the CFR assessed by cardiac magnetic resonance after adenosine infusion in a population of women without obstructive coronary disease [9].


Resolution of angina pectoris and improvement of the coronary flow reserve after ranolazine treatment in a woman with isolated impaired coronary microcirculation.

Santoro A, Schiano Lomoriello V, Santoro C, Muscariello R, Galderisi M - Case Rep Cardiol (2013)

Mechanism of action of ranolazine. The pharmacologically induced reduction of the late sodium current ameliorates the myocardial diastolic relaxation by reducing the diastolic wall stress. This finally produces an improvement of segmental myocardial ischemia.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4008276&req=5

fig6: Mechanism of action of ranolazine. The pharmacologically induced reduction of the late sodium current ameliorates the myocardial diastolic relaxation by reducing the diastolic wall stress. This finally produces an improvement of segmental myocardial ischemia.
Mentions: According to the recommendation of the European Association of Echocardiography [6], the stress echo with dipyridamole represents a very accurate test in order to distinguish an epicardial coronary stenosis from an isolated coronary microvascular dysfunction: the first one shows a reduction of the CFR with impairment of the regional wall motion and the latter shows a reduction of the CFR without regional wall motion abnormalities or even a supernormal wall motion. In our experience a reduced CFR + normal regional wall motion pointed out an impaired function of the coronary microcirculation, where a previous coronary angiography had already shown a coronary three free of stenosis. In this setting, after almost 6 months of therapy, ranolazine caused a relevant rising of the CFR that is strictly linked to its mechanism of action. Ranolazine induces a reduction of the intracellular late sodium current that leads to a reduction of the intracellular calcium concentration thus producing a diastolic relaxation improvement which in its turns enhances the myocardial perfusion [8]. The coronary flow is substantially greater during the diastolic phase of the cardiac cycle thus it is evident that the smaller vessels, the ones that make up the microvascular circulation, are the one that benefit more from the effect of the decompression caused by ranolazine during the myocardial relaxation process. The ranolazine acts therefore as a lusitropic drug that improves the diastolic dysfunction and the segmental ischemia thus affecting one of the first steps of the ischemic cascade (Figure 6). The results of the presented clinical case reflect the ones produced by a recently published clinical study where a 4-week therapy with ranolazine showed to be useful reducing the recurrence of the angina symptoms and improving the CFR assessed by cardiac magnetic resonance after adenosine infusion in a population of women without obstructive coronary disease [9].

Bottom Line: The improvement of both symptoms and coronary microvascular function is strictly linked to the mechanism of action of the drug.Ranolazine induces in fact a reduction of the intracellular late sodium current that leads to a reduction of the intracellular calcium concentration thus producing a better myocardial diastolic relaxation process which in its turns enhances the myocardial perfusion.The ranolazine acts therefore as a lusitropic drug that improves the diastolic dysfunction and the segmental ischemia thus affecting one of the first steps of the ischemic cascade.

View Article: PubMed Central - PubMed

Affiliation: Cardioangiology with CCU, Department of Clinical and Experimental Medicine, Federico II University Hospital, 80131 Naples, Italy.

ABSTRACT
In a 61-year-old woman with well controlled arterial hypertension, hypercholesterolemia, and smoke and suffering from recurrent angina pectoris despite angiographically normal epicardial coronary vessels and maximal therapy, the replacement of nitrates with novel antiangina drug ranolazine, after 6-month therapy, induced a complete relief of angina and a relevant rising of the transthoracic Doppler-derived coronary flow reserve (CFR). The present clinical case underlines therefore how in patients with chronic ischemic heart disease without epicardial coronary stenosis ranolazine can induce an improvement till the complete solution of the angina symptoms and a substantial increase of CFR as expression of the enhancement of the microvascular coronary function. The improvement of both symptoms and coronary microvascular function is strictly linked to the mechanism of action of the drug. Ranolazine induces in fact a reduction of the intracellular late sodium current that leads to a reduction of the intracellular calcium concentration thus producing a better myocardial diastolic relaxation process which in its turns enhances the myocardial perfusion. The ranolazine acts therefore as a lusitropic drug that improves the diastolic dysfunction and the segmental ischemia thus affecting one of the first steps of the ischemic cascade.

No MeSH data available.


Related in: MedlinePlus